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184 results on '"Djouhri, Laiche"'

5. Kv7 Channel Activators Flupirtine and ML213 Alleviate Neuropathic Pain Behavior in the Streptozotocin Rat Model of Diabetic Neuropathy

Author

Ahmed,Ashraf, Al-Nuaimi,Salma, Mustafa,Ayman, Zeidan,Asad, Agouni,Abdelali, Djouhri,Laiche, Ahmed,Ashraf, Al-Nuaimi,Salma, Mustafa,Ayman, Zeidan,Asad, Agouni,Abdelali, and Djouhri,Laiche

Abstract

Ashraf Ibrahim Ahmed,1 Salma Al-Nuaimi,1 Ayman Mustafa,1 Asad Zeidan,1 Abdelali Agouni,2 Laiche Djouhri1 1Department of Basic Medical Science, College of Medicine, QU Health, Qatar University, Doha, Qatar; 2Department of Pharmaceutical Sciences, College of Pharmacy, QU health, Qatar University, Doha, QatarCorrespondence: Laiche Djouhri, Email ldjouhri@qu.edu.qaBackground & Objective: Chronic peripheral neuropathic pain (PNP) is a debilitating condition that is associated with many types of injury/diseases, including diabetes mellitus. Patients with longstanding diabetes develop diabetic PNP (DPNP), which is resilient to currently available drugs. The underlying molecular mechanisms of DPNP are still illusive, but Kv 7 channels that have been implicated in the pathogenesis of various types of chronic pain are likely to be involved. Indeed, using the streptozotocin (STZ) rat model of DPNP, we have previously shown that Kv 7 activation with their non-selective activator retigabine attenuated neuropathic pain behavior suggesting that these channels are implicated in DPNP pathogenesis. Here, we evaluated, in the same STZ model, whether the more potent and more selective Kv 7 channel openers flupirtine and ML213 attenuate STZ-induced pain hypersensitivity.Methods: Male Sprague Dawley rats (250– 300 g) were used. The STZ model involved a single injection of STZ (60 mg/kg, i.p.). Behavioral testing for mechanical and heat pain sensitivity was performed using a dynamic plantar aesthesiometer and Hargreaves analgesiometer, respectively.Results: STZ rats exhibited behavioral signs of mechanical and heat hypersensitivity as indicated by significant decreases in the mean paw withdrawal threshold (PWT) and mean paw withdrawal latency (PWL), respectively, at 35 days post-STZ treatment. Single injections of flupirtine (10 mg/kg, i.p.) and ML213 (5 mg/kg, i.p.) to STZ rats (35-days after STZ treatment) caused significant increases in the mean PWT, but not PWL, indicating atten

Published
2024

9. Kv7 Channel Activators Flupirtine and ML213 Alleviate Neuropathic Pain Behavior in the Streptozotocin Rat Model of Diabetic Neuropathy.

Author

Ahmed, Ashraf Ibrahim, Al-Nuaimi, Salma, Mustafa, Ayman, Zeidan, Asad, Agouni, Abdelali, and Djouhri, Laiche

Subjects
SPRAGUE Dawley rats, LABORATORY rats, DIABETIC neuropathies, NEURALGIA, ION channels
Abstract

Chronic peripheral neuropathic pain (PNP) is a debilitating condition that is associated with many types of injury/diseases, including diabetes mellitus. Patients with longstanding diabetes develop diabetic PNP (DPNP), which is resilient to currently available drugs. The underlying molecular mechanisms of DPNP are still illusive, but Kv 7 channels that have been implicated in the pathogenesis of various types of chronic pain are likely to be involved. Indeed, using the streptozotocin (STZ) rat model of DPNP, we have previously shown that Kv 7 activation with their non-selective activator retigabine attenuated neuropathic pain behavior suggesting that these channels are implicated in DPNP pathogenesis. Here, we evaluated, in the same STZ model, whether the more potent and more selective Kv 7 channel openers flupirtine and ML213 attenuate STZ-induced pain hypersensitivity. Methods: Male Sprague Dawley rats (250– 300 g) were used. The STZ model involved a single injection of STZ (60 mg/kg, i.p.). Behavioral testing for mechanical and heat pain sensitivity was performed using a dynamic plantar aesthesiometer and Hargreaves analgesiometer, respectively. Results: STZ rats exhibited behavioral signs of mechanical and heat hypersensitivity as indicated by significant decreases in the mean paw withdrawal threshold (PWT) and mean paw withdrawal latency (PWL), respectively, at 35 days post-STZ treatment. Single injections of flupirtine (10 mg/kg, i.p.) and ML213 (5 mg/kg, i.p.) to STZ rats (35-days after STZ treatment) caused significant increases in the mean PWT, but not PWL, indicating attenuation of mechanical, but not heat hypersensitivity. Both flupirtine and ML213 were as effective as the positive control gabapentin (10/kg, i.p.), and their anti-allodynic effects were prevented by the Kv 7 channel-specific blocker XE991 (3 mg/kg, i.p.). Conclusion: The findings suggest that Kv 7 channels are involved in the mechanisms of mechanical but not heat hypersensitivity associated with DPNP, and that their activation may prove to be effective in alleviating DPNP symptoms. [ABSTRACT FROM AUTHOR]

Published
2024
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11. Association Between Metabolic Syndrome and Decline in Cognitive Function: A Cross-Sectional Study

Author

Alsuwaidi,Hissa N, Ahmed,Ashraf, Alkorbi,Hamad A, Ali,Sara M, Altarawneh,Lina N, Uddin,Shooq I, Roueentan,Sara R, Alhitmi,Asmaa A, Djouhri,Laiche, Chivese,Tawanda, Alsuwaidi,Hissa N, Ahmed,Ashraf, Alkorbi,Hamad A, Ali,Sara M, Altarawneh,Lina N, Uddin,Shooq I, Roueentan,Sara R, Alhitmi,Asmaa A, Djouhri,Laiche, and Chivese,Tawanda

Abstract

Hissa N Alsuwaidi,* Ashraf I Ahmed,* Hamad A Alkorbi, Sara M Ali, Lina N Altarawneh, Shooq I Uddin, Sara R Roueentan, Asmaa A Alhitmi, Laiche Djouhri, Tawanda Chivese College of Medicine, QU Health, Qatar University, Doha, Qatar*These authors contributed equally to this workCorrespondence: Tawanda Chivese, College of Medicine, Qatar University, PO BOX, Doha, 2713, Qatar, Email tchivese@qu.edu.qaAim: We investigated whether metabolic syndrome (MetS) is associated with a decline in cognitive function in a cohort of middle-aged and elderly individuals without known cognitive dysfunction diseases in Qatar.Methods: We conducted a cross-sectional study on randomly selected participants aged 40– 80 years from the Qatar Biobank, with data on cognitive tests and MetS components. Participants with a history of dementia, stroke, or mental disorders were excluded. MetS was diagnosed using the NCEP-ATP III criteria and cognitive performance was assessed using the Cambridge Neuropsychological Test Automated Battery (CANTAB). Two cognitive function domains were assessed. These are speed of reaction, measured using the Reaction Time (RT), and short-term visual memory, measured using the Paired Associate Learning (PAL) test. Multivariable logistic regression models were used to determine associations between MetS and poor speed of reaction and poor memory performance.Results: The mean age of the participants included was 49.8 years (SD 6.7). Of these, 51.9% were females and 88.0% were of Qatari nationality. Most of the 1000 participants had MetS (n=302) or 1– 2 MetS components (n=523), whereas only 170 had no MetS components. There was a strong association between MetS and poor memory performance (OR 1.76, 95% CI 1.04– 2.96, P=0.034), but a weaker association with poor speed of reaction (OR 1.5, 95% CI 0.89– 2.50, P=0.125).Conclusion: In middle-aged and elderly individuals, MetS was strongly associated with diminished short-term visual memory, psychom

Published
2023

12. Umbelliferone Inhibits Spermatogenic Defects and Testicular Injury in Lead-Intoxicated Rats by Suppressing Oxidative Stress and Inflammation, and Improving Nrf2/HO-1 Signaling [Retraction]

Author

Alotaibi,Mohammed F, Al-Joufi,Fakhria, Abou Seif,Howida S, Alzoghaibi,Mohammed A, Djouhri,Laiche, Ahmeda,Ahmad F, Mahmoud,Ayman M, Alotaibi,Mohammed F, Al-Joufi,Fakhria, Abou Seif,Howida S, Alzoghaibi,Mohammed A, Djouhri,Laiche, Ahmeda,Ahmad F, and Mahmoud,Ayman M

Abstract

Alotaibi MF, Al-Joufi F, Abou Seif HS, et al. Drug Des Devel Ther. 2020;14:4003-4019 The Editor and Publisher of Drug Design, Development and Therapy are retracting the published article. Concerns were raised regarding the duplication of images in Figure 2 and an investigation found overlap in the images for Figures 2D and 2E, despite both images representing results of different treatments. The authors cooperated with the investigation and provided data associated with the reported study. However, despite the authors’ assistance, a satisfactory explanation for how the images came to be duplicated could not be provided, and the validity of the published work could not be verified. The decision was made to retract the article and the authors were notified of this. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”.

Published
2023

19. Between Inflammation and Autophagy: The Role of Leptin-Adiponectin Axis in Cardiac Remodeling

Author

Kamareddine,Layla, Ghantous,Crystal M, Allouch,Soumaya, Al-Ashmar,Sarah A, Anlar,Gulsen, Kannan,Surya, Djouhri,Laiche, Korashy,Hesham M, Agouni,Abdelali, and Zeidan,Asad

Subjects
Journal of Inflammation Research
Abstract

Layla Kamareddine,1– 3 Crystal M Ghantous,4 Soumaya Allouch,5 Sarah A Al-Ashmar,2,5 Gulsen Anlar,2,5 Surya Kannan,2,5 Laiche Djouhri,2,5 Hesham M Korashy,2,6 Abdelali Agouni,2,6 Asad Zeidan2,5 1Department Biomedical Sciences, College of Health Sciences, QU Health, Qatar University, Doha, Qatar; 2Biomedical and Pharmaceutical Research Unit, QU Health, Qatar University, Doha, Qatar; 3Biomedical Research Center, Qatar University, Doha, Qatar; 4Department of Nursing and Health Sciences, Faculty of Nursing and Health Sciences, Notre Dame University-Louaize, Keserwan, Lebanon; 5Department of Basic Sciences, College of Medicine, QU Health, Qatar University, Doha, Qatar; 6Department of Pharmaceutical Sciences, College of Pharmacy, QU Health, Qatar University, Doha, QatarCorrespondence: Asad ZeidanDepartment of Basic Sciences, College of Medicine, QU Health, Qatar University, Doha, QatarEmail a.zeidan@qu.edu.qaAbstract: Cardiac remodeling is the process by which the heart adapts to stressful stimuli, such as hypertension and ischemia/reperfusion; it ultimately leads to heart failure upon long-term exposure. Autophagy, a cellular catabolic process that was originally considered as a mechanism of cell death in response to detrimental stimuli, is thought to be one of the main mechanisms that controls cardiac remodeling and induces heart failure. Dysregulation of the adipokines leptin and adiponectin, which plays essential roles in lipid and glucose metabolism, and in the pathophysiology of the neuroendocrine and cardiovascular systems, has been shown to affect the autophagic response in the heart and to contribute to accelerate cardiac remodeling. The obesity-associated protein leptin is a pro-inflammatory, tumor-promoting adipocytokine whose elevated levels in obesity are associated with acute cardiovascular events, and obesity-related hypertension. Adiponectin exerts anti-inflammatory and anti-tumor effects, and its reduced levels in obesity correlate with the pathogenesis of obesity-associated cardiovascular diseases. Leptin- and adiponectin-induced changes in autophagic flux have been linked to cardiac remodeling and heart failure. In this review, we describe the different molecular mechanisms of hyperleptinemia- and hypoadiponectinemia-mediated pathogenesis of cardiac remodeling and the involvement of autophagy in this process. A better understanding of the roles of leptin, adiponectin, and autophagy in cardiac functions and remodeling, and the exact signal transduction pathways by which they contribute to cardiac diseases may well lead to discovery of new therapeutic agents for the treatment of cardiovascular remodeling.Keywords: inflammation, autophagy, leptin, adiponectin, cardiac cells

Published
2021

20. Follicular dendritic cells

Author

Abd El‐Aleem, Seham A., primary, Saber, Entesar Ali, additional, Aziz, Neven M., additional, El‐Sherif, Hani, additional, Abdelraof, Asmaa M., additional, and Djouhri, Laiche, additional

Published
2021
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22. A Golgi study of neurons in the camel cerebellum (Camelus dromedarius)

Author

Al-Hussain, Saleh M., Yousuf, Mustafa S., Hani, Ayat Bani, Zaqout, Sami, Djouhri, Laiche, and Mustafa, Ayman G.

Subjects
camel, nervous system, cerebellum, Golgi, neurons
Abstract

Neurons in the cerebellar cortex of camels were studied using modified Golgi impregnation methods. Neurons were classified according to their position, morphology of their soma, density and distribution of dendrites, and the course of their axons. Accordingly, eight types of neurons were identified. Three types were found in the molecular layer: upper and lower stellate cells and basket cells, and four types were found in the granular layer: granule cells, Golgi Type II cells, Lugaro cells, and unipolar brush cells. Only the somata of Purkinje cells were found in the Purkinje cell layer. The molecular layer is characterized by the presence of more dendrites, dendritic spines, and transverse fibers. Golgi cells also show extensive dendritic branching and spines. The results illustrate the neuronal features of the camel cerebellum as a large mammal living in harsh environmental conditions. These findings should contribute to advancing our understanding of species-comparative anatomy in achieving better coordination of motor activity.

Published
2021

25. Follicular dendritic cells.

Author

Abd El‐Aleem, Seham A., Saber, Entesar Ali, Aziz, Neven M., El‐Sherif, Hani, Abdelraof, Asmaa M., and Djouhri, Laiche

Subjects
IMMUNOREGULATION, ANTIGEN presenting cells, B cells, LYMPHOID tissue, HUMORAL immunity, FOLLICULAR dendritic cells, PRION diseases
Abstract

Follicular dendritic cells (FDCs) are unique accessory immune cells that contribute to the regulation of humoral immunity. They are multitasker cells essential for the organization and maintenance of the lymphoid architecture, induction of germinal center reaction, production of B memory cells, and protection from autoimmune disorders. They perform their activities through both antigen‐driven and chemical signaling to B cells. FDCs play a crucial role in the physiological regulation of the immune response. Dis‐regulation of this immune response results when FDCs retain antigens for years. This provides a constant antigenic stimulation for B cells resulting in the development of immune disorders. Antigen trapped on FDCs is resistant to therapeutic intervention causing chronicity and recurrences. Beyond their physiological immunoregulatory functions, FDCs are involved in the pathogenesis of several immune‐related disorders including HIV/AIDS, prion diseases, chronic inflammatory, and autoimmune disorders. FDCs have also been recently implicated in rare neoplasms of lymphoid and hematopoietic tissues. Understanding FDC biology is essential for better control of humoral immunity and opens the gate for therapeutic management of FDC‐mediated immune disorders. Thus, the biology of FDCs has become a hot research area in the last couple of decades. In this review, we aim to provide a comprehensive overview of FDCs and their role in physiological and pathological conditions. [ABSTRACT FROM AUTHOR]

Published
2022
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27. Molecular Mechanisms of Adiponectin-Induced Attenuation of Mechanical Stretch-Mediated Vascular Remodeling

Author

Ghantous, Crystal M., Farhat, Rima, Djouhri, Laiche, Alashmar, Sarah, Anlar, Gulsen, Korashy, Hesham M., Agouni, Abdelali, and Zeidan, Asad

Subjects
Leptin, Male, animal structures, Article Subject, Nitric Oxide Synthase Type III, Myocytes, Smooth Muscle, Protein Serine-Threonine Kinases, Vascular Remodeling, leptin, Muscle, Smooth, Vascular, Rats, Sprague-Dawley, AMP-Activated Protein Kinase Kinases, Animals, RNA, Messenger, Phosphorylation, Extracellular Signal-Regulated MAP Kinases, Cell Nucleus, QH573-671, adiponectin, Portal Vein, Adenylate Kinase, Hypertrophy, GATA4 Transcription Factor, Biological sciences, FOS: Biological sciences, Biochemistry and cell biology, Hypertension, Adiponectin, Stress, Mechanical, Receptors, Adiponectin, Cytology, Reactive Oxygen Species, hormones, hormone substitutes, and hormone antagonists, Research Article
Abstract

Hypertension induces vascular hypertrophy, which changes blood vessels structurally and functionally, leading to reduced tissue perfusion and further hypertension. It is also associated with dysregulated levels of the circulating adipokines leptin and adiponectin (APN). Leptin is an obesity-associated hormone that promotes vascular smooth muscle cell (VSMC) hypertrophy. APN is a cardioprotective hormone that has been shown to attenuate hypertrophic cardiomyopathy. In this study, we investigated the molecular mechanisms of hypertension-induced VSMC remodeling and the involvement of leptin and APN in this process. To mimic hypertension, the rat portal vein (RPV) was mechanically stretched, and the protective effects of APN on mechanical stretch-induced vascular remodeling and the molecular mechanisms involved were examined by using 10μg/ml APN. Mechanically stretching the RPV significantly decreased APN protein expression after 24 hours and APN mRNA expression in a time-dependent manner in VSMCs. The mRNA expression of the APN receptors AdipoR1, AdipoR2, and Tcadherin significantly increased after 15 hours of stretch. The ratio of APN/leptin expression in VSMCs significantly decreased after 24 hours of mechanical stretch. Stretching the RPV for 3 days increased the weight and [3H]-leucine incorporation significantly, whereas APN significantly reduced hypertrophy in mechanically stretched vessels. Stretching the RPV for 10 minutes significantly decreased phosphorylation of LKB1, AMPK, and eNOS, while APN significantly increased p-LKB1, pAMPK, and p-eNOS in stretched vessels. Mechanical stretch significantly increased p-ERK1/2 after 10 minutes, whereas APN significantly reduced stretch-induced ERK1/2 phosphorylation. Stretching the RPV also significantly increased ROS generation after 1 hour, whereas APN significantly decreased mechanical stretch-induced ROS production. Exogenous leptin (3.1nM) markedly increased GATA-4 nuclear translocation in VSMCs, whereas APN significantly attenuated leptin-induced GATA-4 nuclear translocation. Our results decipher molecular mechanisms of APN-induced attenuation of mechanical stretch-mediated vascular hypertrophy, with the promising potential of ultimately translating this protective hormone into the clinic. This work was supported by the Medical Practice Plan (MPP), Faculty of Medicine at AUB to AZ, the National Council for Scientific Research of Lebanon (CNRS-L) to CMG, and the graduate teaching/research assistantship support from Qatar University to SA. The publication of this article was funded by the Qatar National Library.

Published
2020

28. RETRACTED ARTICLE: Umbelliferone Inhibits Spermatogenic Defects and Testicular Injury in Lead-Intoxicated Rats by Suppressing Oxidative Stress and Inflammation, and Improving Nrf2/HO-1 Signaling

Author

Alotaibi,Mohammed F, Al-Joufi,Fakhria, Abou Seif,Howida S, Alzoghaibi,Mohammed A, Djouhri,Laiche, Ahmeda,Ahmad F, Mahmoud,Ayman M, Alotaibi,Mohammed F, Al-Joufi,Fakhria, Abou Seif,Howida S, Alzoghaibi,Mohammed A, Djouhri,Laiche, Ahmeda,Ahmad F, and Mahmoud,Ayman M

Abstract

This paper has been retracted. Alotaibi MF, Al-Joufi F, Abou Seif HS, et al. Drug Des Devel Ther. 2020;14:4003-4019 The Editor and Publisher of Drug Design, Development and Therapy are retracting the published article. Concerns were raised regarding the duplication of images in Figure 2 and an investigation found overlap in the images for Figures 2D and 2E, despite both images representing results of different treatments. The authors cooperated with the investigation and provided data associated with the reported study. However, despite the authors’ assistance, a satisfactory explanation for how the images came to be duplicated could not be provided, and the validity of the published work could not be verified. The decision was made to retract the article and the authors were notified of this. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as “Retracted”.

Published
2020

37. CD28 Superagonistic Activation of T Cells Induces a Tumor Cell-Like Metabolic Program

Author

Thaventhiran, Thilipan, primary, Wong, Wai, additional, Alghanem, Ahmad F., additional, Alhumeed, Naif, additional, Aljasir, Mohammad A., additional, Ramsey, Simeon, additional, Sethu, Swaminathan, additional, Aw Yeang, Han Xian, additional, Chadwick, Amy E., additional, Cross, Michael, additional, Webb, Steven D., additional, Djouhri, Laiche, additional, Ball, Christina, additional, Stebbings, Richard, additional, and Sathish, Jean G., additional

Published
2019
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39. Activation of Kv7 channels with the anticonvulsant retigabine alleviates neuropathic pain behaviour in the streptozotocin rat model of diabetic neuropathy.

Author

Djouhri, Laiche, Malki, Mohammed Imad, Zeidan, Asad, Nagi, Karim, and Smith, Trevor

Subjects
*DIABETIC neuropathies, *PERIPHERAL neuropathy, *HEAT stroke, *RATS, *DIABETES complications, *PAIN
Abstract

Diabetic peripheral neuropathy (DPN) is the most incapacitating complication of diabetes mellitus. Up to 50% of patients with DPN develop peripheral neuropathic pain (PNP). The underlying ionic and molecular mechanisms of diabetic PNP (DPNP) are poorly understood. However, voltage gated potassium (Kv7) channels which have been implicated in the pathogenesis of other types of PNP are likely to be involved. Here we examined, in the streptozotocin (STZ) rat model of DPNP, whether activating the Kv7 channels with a potent activator retigabine (ezogabine) would reverse/attenuate behavioural signs of DPNP. STZ rats exhibited behavioural indices of mechanical and heat hypersensitivity, but not cold hypersensitivity or spontaneous pain, 35 days after STZ injection. Retigabine given at a dose of 15 mg/kg (but not at 7.5 mg/kg, i.p.) significantly attenuated mechanical, but not heat hypersensitivity in DPNP rats, and was as effective as the positive control gabapentin. This analgesic effect of retigabine was completely reversed by the Kv7/M channel blocker XE991 (3 mg/kg, i.p.) indicating that the anti-allodynic effects of retigabine were mediated by Kv7 channels. In conclusion, the findings suggest that Kv7 channels are involved in DPNP pathogenesis, and that strategies that target their activation may prove to be effective in treating DPNP. [ABSTRACT FROM AUTHOR]

Published
2019
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41. Abstracts from the 3rd International Genomic Medicine Conference (3rd IGMC 2015)

Author

Jerry W. Shay, Noriko Homma, Ruyun Zhou, Muhammad Imran Naseer, Adeel G. Chaudhary, Mohammed Al-Qahtani, Nobutaka Hirokawa, Maryam Goudarzi, Albert J. Fornace, Saleh Baeesa, Deema Hussain, Mohammed Bangash, Fahad Alghamdi, Hans-Juergen Schulten, Angel Carracedo, Ishaq Khan, Hanadi Qashqari, Nawal Madkhali, Mohamad Saka, Kulvinder S. Saini, Awatif Jamal, Jaudah Al-Maghrabi, Adel Abuzenadah, Adeel Chaudhary, Mohammed Al Qahtani, Ghazi Damanhouri, Heba Alkhatabi, Anne Goodeve, Laura Crookes, Nikolas Niksic, Nicholas Beauchamp, Adel M. Abuzenadah, Jim Vaught, Bruce Budowle, Mourad Assidi, Abdelbaset Buhmeida, Leena Merdad, Sudhir Kumar, Sayaka Miura, Karen Gomez, Mahmood Rasool, Ahmed Rebai, Sajjad Karim, Hend F. Nour Eldin, Heba Abusamra, Elham M. Alhathli, Nada Salem, Mohammed H. Al-Qahtani, Hossam Faheem, Ashok Agarwa, Eberhard Nieschlag, Joachim Wistuba, Oliver S. Damm, Mohd A. Beg, Taha A. Abdel-Meguid, Hisham A. Mosli, Osama S. Bajouh, Serdar Coskun, Muhammad Abu-Elmagd, Ashraf Dallol, Sahar Hakamy, Wejdan Al-Qahtani, Asia Al-Harbi, Shireen Hussain, Burak Ozkosem, Rick DuBois, Safia S. Messaoudi, Maryam T. Dandana, Touhami Mahjoub, Wassim Y. Almawi, S. Abdalla, M. Nabil Al-Aama, Asmaa Elzawahry, Tsuyoshi Takahashi, Sachiyo Mimaki, Eisaku Furukawa, Rie Nakatsuka, Isao Kurosaka, Takahiko Nishigaki, Hiromi Nakamura, Satoshi Serada, Tetsuji Naka, Seiichi Hirota, Tatsuhiro Shibata, Katsuya Tsuchihara, Toshirou Nishida, Mamoru Kato, Sajid Mehmood, Naeem Mahmood Ashraf, Awais Asif, Muhammad Bilal, Malik Siddique Mehmood, Aadil Hussain, Qazi Mohammad Sajid Jamal, Mughees Uddin Siddiqui, Mohammad A. Alzohairy, Mohammad A. Al Karaawi, Taoufik Nedjadi, Heba Al-Khattabi, Adel Al-Ammari, Ahmed Al-Sayyad, Hédia Zitouni, Nozha Raguema, Marwa Ben Ali, Wided Malah, Raja Lfalah, Wassim Almawi, Mohammed Elanbari, Andrey Ptitsyn, Sana Mahjoub, Rabeb El Ghali, Bechir Achour, Nidhal Ben Amor, Brahim N’siri, Hamid Morjani, Esam Azhar, Vera Chayeb, Maryam Dendena, Hedia Zitouni, Khedija Zouari-Limayem, Bassem Refaat, Ahmed M. Ashshi, Sarah A. Batwa, Hazem Ramadan, Amal Awad, Ahmed Ateya, Adel Galal Ahmed El-Shemi, Ahmad Ashshi, Mohammed Basalamah, Youjin Na, Chae-Ok Yun, Adel Galal El-Shemi, Osama Kensara, Amr Abdelfattah, Batol Imran Dheeb, Mohammed M. F. Al-Halbosiy, Rghad Kadhim Al lihabi, Basim Mohammed Khashman, Djouhri Laiche, Chaudhary Adeel, Nedjadi Taoufik, Hani Al-Afghani, Maria Łastowska, Haya H. Al-Balool, Harsh Sheth, Emma Mercer, Jonathan M. Coxhead, Chris P. F. Redfern, Heiko Peters, Alastair D. Burt, Mauro Santibanez-Koref, Chris M. Bacon, Louis Chesler, Alistair G. Rust, David J. Adams, Daniel Williamson, Steven C. Clifford, Michael S. Jackson, Mala Singh, Mohmmad Shoab Mansuri, Shahnawaz D. Jadeja, Hima Patel, Yogesh S. Marfatia, Rasheedunnisa Begum, Amal M. Mohamed, Alaa K. Kamel, Nivin A. Helmy, Sayda A. Hammad, Hesham F. Kayed, Marwa I. Shehab, Assad El Gerzawy, Maha M. Ead, Ola M. Ead, Mona Mekkawy, Innas Mazen, Mona El-Ruby, S. M. A. Shahid, J. M. Arif, Mohtashim Lohani, Moumni Imen, Chaouch Leila, Ouragini Houyem, Douzi Kais, Chaouachi Dorra Mellouli Fethi, Bejaoui Mohamed, Abbes Salem, Areeg Faggad, Amanuel T. Gebreslasie, Hani Y. Zaki, Badreldin E. Abdalla, Maha S. AlShammari, Rhaya Al-Ali, Nader Al-Balawi, Mansour Al-Enazi, Ali Al-Muraikhi, Fadi Busaleh, Ali Al-Sahwan, Francis Borgio, Abdulazeez Sayyed, Amein Al-Ali, Sadananda Acharya, Maha S. Zaki, Hala T. El-Bassyouni, Mohammed F. Elshal, Kaleemuddin M., Alia M. Aldahlawi, Omar Saadah, J. Philip McCoy, Adel E. El-Tarras, Nabil S. Awad, Abdulla A. Alharthi, Mohamed M. M. Ibrahim, Haneen S. Alsehli, Abdullah M. Gari, Mohammed M. Abbas, Roaa A. Kadam, Mazen M. Gari, Mohmmed H. Alkaff, Mamdooh A. Gari, Hend F. Nour eldin, Fatima A. Moradi, Omran M. Rashidi, Zuhier A. Awan, Ibrahim Hamza Kaya, Olfat Al-Harazi, Dilek Colak, Nabila A. Alkousi, Takis Athanasopoulos, Afnan O. Bahmaid, Etimad A. Alhwait, Mohammed H. Alkaf, Roaa Kadam, Gauthaman Kalamegam, Elham Alhathli, Salma N. Alsayed, Fawziah H. Aljohani, Samaher M. Habeeb, Rawan A. Almashali, Sulman Basit, Samia M. Ahmed, Rakesh Sharma, Ashok Agarwal, Damayanthi Durairajanayagam, Luna Samanta, Edmund S. Sabanegh, Zhihong Cui, Alaa A. Alboogmi, Nuha A. Alansari, Maha M. Al-Quaiti, Fai T. Ashgan, Afnan Bandah, Hasan S. Jamal, Abdullraheem Rozi, Zeenat Mirza, Ahmad J. Al Sayyad, Hasan M. A. Farsi, Jaudah A. Al-Maghrabi, Reem Alotibi, Alaa Al-Ahmadi, Alaa A. Albogmi, Rasha A. Ebiya, Samia M. Darwish, Metwally M. Montaser, Vladimir B. Bajic, Wafaey Gomaa, Mehenaz Hanbazazh, Mahmoud Al-Ahwal, Saher Hakamy, Ghali Baba, Abdullah Al-Harbi, Ghalia Baba, Hend Nour Eldin, Aisha A. Alyamani, Rawan Gadi, Saadiah M. Alfakeeh, Rubi Ghazala, Shilu Mathew, M. Haroon Hamed, Ishtiaq Qadri, Lobna Mira, Manal Shaabad, Mikhlid H. Almutairi, Angie Ambers, Jennifer Churchill, Jonathan King, Monika Stoljarova, Harrell Gill-King, Muhammad Al-Qatani, Farid Ahmed, Taha Abo Almagd, Muhammad Al-Qahtani, Abdelbaset Buhmaida, Rukhsana Satar, Waseem Ahmad, Nazia Nazam, Mohamad I. Lone, Muhammad I. Naseer, Mohammad S. Jamal, Syed K. Zaidi, Peter N. Pushparaj, Mohammad A. Jafri, Shakeel A. Ansari, Mohammed H. Alqahtani, Hanan Bashier, Abrar Al Qahtani, Amal M. Nour, Adel M. Abu Zenadah, Muhammed Al Qahtani, Muhammad Faheem, Shiny Mathew, Peter Natesan Pushparaj, Mohammad H. Al-Qahtani, Hani A. Alhadrami, Ibtessam R. Hussein, Rima S. Bader, Randa Bassiouni, Maha Alquaiti, Fai Ashgan, Hans Schulten, Mohamed Nabil Alama, Mohammad H. Al Qahtani, Mohammad I. Lone, Nazia Nizam, Muhammed H. Al-Qahtani, Eradah Alshihri, Lina Alharbi, Peter Pushparaj Natesan, Fazal Khan, Khalid Hussain Wali Sait, Nisreen Anfinan, Lobna S. Mira, Mohammed H. AlQahtani, Sameera Sogaty, Randa I. Bassiouni, Abdulrahman M. S. Sibiani, Mohiuddin K. Warsi, null Rubi, Kundan Kumar, Ahmad A. T. Naqvi, Faizan Ahmad, Md I. Hassan, Ashraf Ali, Jummanah Jarullah, Abdelbasit Buhmeida, Shahida Khan, Ghufrana Abdussami, Maryam Mahfooz, Mohammad A. Kamal, Ghazi A. Damanhouri, Bushra Jarullah, Mohammad S. S. Jarullah, Osama Bajouh, Abdulah E. A. Mathkoor, Hashim M. A. Alsalmi, Anas M. M. Oun, Ghazi A. Damanhauri, Adeel G. Chudhary, Yousif A. Abutalib, Daniele Merico, Susan Walker, Christian R. Marshall, Mehdi Zarrei, Stephen W. Scherer, Fai Talal Ashgan, Syed Kashif Zaidi, Mohammed M. Jan, Maryam Al-Zahrani, Sahira Lary, Emmanuel Dermitzakis, Abeer A. Al-refai, Mona Saleh, Rehab I. Yassien, Mahmmoud Kamel, Rabab M. Habeb, Najlaa Filimban, Nadia Ghannam, Adel Mohammed Abuzenadah, Fehmida Bibi, Sana Akhtar, Esam I. Azhar, Muhammad Yasir, Muhammad I. Nasser, Asif A. Jiman-Fatani, Ali Sawan, Ruaa A. Lahzah, Asho Ali, Syed A. Hassan, Seyed E. Hasnain, Iftikhar A. Tayubi, Hamza A. Abujabal, Alaa O. Magrabi, Adel Abuzenada, Taha Abduallah Kumosani, Elie Barbour, Manal Shabaad, Adnan Merdad, Kalamegam Gauthaman, Mamdooh Gari, Hani M. A. Aljahdali, Reham Al Nono, Haneen Alsehli, Mohammed Abbas, Mohammed Sarwar Jamal, Shakeel Ansari, Mansour A. Alghamdi, Magdy Shamy, Max Costa, Mamdouh I. Khoder, Najla Kharrat, Sabrine Belmabrouk, Rania Abdelhedi, Riadh Benmarzoug, Mohammed H. Al Qahtani, Ghazi Dhamanhouri, Abdelwahab Noorwali, Mohammad Khalid Alwasiyah, Afnan Bahamaid, Saadiah Alfakeeh, Aisha Alyamani, Ali Mobasheri, Mohammad Sarwar Jamal, Raziuddin Khan, Kanchan Bhatia, Saif Ahmad, Iftikhar AslamTayubi, Manish Tripathi, Syed Asif Hassan, Rahul Shrivastava, Syed Hassan, Hamza A. S. Abujabal, Ishani Shah, Ishfaq A. Sheikh, Ejaz Ahmad, Mohd Rehan, Samera F. AlBasri, Rola F. Turki, Sahar A. F. Hammoudah, Khalid M. AlHarbi, Lama M. El-Attar, Ahmed M. Z. Darwish, Sara M. Ibrahim, Hani Choudhry, Jalaludden Awlia, Imran khan, Sameera Al-basri, Taha Kumosani, Heba M. EL Sayed, Eman A. Hafez, Aisha Hassan Elaimi, Randa Ibrahim Bassiouni, Richard F. Wintle, Vikram Gopalakrishna Pillai, Sujata Sharma, Punit Kaur, Alagiri Srinivasan, Tej P. Singh, Fatima Al-Adwani, Deema Hussein, Mona Al-Sharif, Fahad Al-Ghamdi, Saleh S. Baeesa, Taha Abdullah Kumosani, Faisal A. Al-Allaf, Zainularifeen Abduljaleel, Abdullah Alashwal, Mohiuddin M. Taher, Abdellatif Bouazzaoui, Halah Abalkhail, Faisal A. Ba-Hammam, Mohammad Athar, Khalid HussainWali Sait, Naira Ben Mami, Yosr Z. Haffani, Mouna Medhioub, Lamine Hamzaoui, Ameur Cherif, Msadok Azouz, Mohammed Imran Nasser, Shereen A. Turkistany, Lina M. Al-harbi, Jamal Sabir, Basmah Al-Madoudi, Bayan Al-Aslani, Khulud Al-Harbi, Rwan Al-Jahdali, Hanadi Qudaih, Emad Al Hamzy, Asad M. Ilyas, Youssri Ahmed, Mohammed Alqahtani, Alaa Alamandi, Ohoud Subhi, Nadia Bagatian, Adel Al-Johari, Osman Abdel Al-Hamour, Hosam Al-Aradati, Abdulmonem Al-Mutawa, Faisal Al-Mashat, Mohammad Al-Qahtani, Muhammad W. shah, Esam I Azhar, Saad Al-Masoodi, Emna Khamla, Chaima Jlassi, Ahmed S. Masmoudi, Lassaad Belbahri, Shadi Al-Khayyat, Roba Attas, Atlal Abu-Sanad, Mohammed Abuzinadah, Habib Bouazzi, Carlos Trujillo, Maha Alotaibi, Rami Nassir, Essam H. Jiffri, Ghulam M. Ashraf, Mohammad A. Aziz, Rizwan Ali, Nusaibah Samman, Sathish Periyasamy, Mohammed Aldress, Majed Al Otaibi, Zeyad Al Yousef, Mohamed Boudjelal, Ibrahim AlAbdulkarim, Mohd Suhail, Abid Qureshi, Adil Jamal, Mahmoud Z. El-Readi, Safaa Y. Eid, Michael Wink, Ahmed M. Isa, Lulu Alnuaim, Johara Almutawa, Basim Abu-Rafae, Saleh Alasiri, Saleh Binsaleh, and Mohamed H. Alqahtani

Subjects
0301 basic medicine, 03 medical and health sciences, 030104 developmental biology, Differentially expressed genes, Gene expression, Genetics, Feature selection, Computational biology, Biology, Cluster analysis, Classifier (UML), Biotechnology
Published
2016

44. TREK2 Expressed Selectively in IB4-Binding C-Fiber Nociceptors Hyperpolarizes Their Membrane Potentials and Limits Spontaneous Pain

Author

Acosta, Cristian, Djouhri, Laiche, Watkins, Roger, Berry, Carol, Bromage, Kirsty, and Lawson, Sally N.

Subjects
Blotting, Western, Nociceptors, Articles, Immunohistochemistry, Membrane Potentials, Rats, Electrophysiology, Disease Models, Animal, Potassium Channels, Tandem Pore Domain, nervous system, Ganglia, Spinal, Gene Knockdown Techniques, Animals, Neuralgia, Female, Rats, Wistar
Abstract

Ongoing/spontaneous pain behavior is associated with ongoing/spontaneous firing (SF) in adult DRG C-fiber nociceptors (Djouhri et al., 2006). Causes of this SF are not understood. We show here that conducting (sometimes called uninjured) C-nociceptors in neuropathic pain models with more hyperpolarized resting membrane potentials (Ems) have lower SF rates. Understanding the control of their Ems may therefore be important for limiting pathological pain. We report that TREK2, a leak K(+) channel, is selectively expressed in IB4 binding rat C-nociceptors. These IB4(+) C-neurons are ∼10 mV more hyperpolarized than IB4(-) C-neurons in vivo (Fang et al., 2006). TREK2 knockdown by siRNA in these neurons in culture depolarized them by ∼10 mV, suggesting that TREK2 is responsible for this ∼10 mV difference. In vivo, more hyperpolarized C-nociceptor Ems were associated with higher cytoplasmic edge-TREK2 expression (edge-TREK2). Edge-TREK2 decreased in C-neurons 7 d after axotomy, and their Ems depolarized by ∼10 mV. This again supports a contribution of TREK2 to their Ems. These relationships between (1) Em and TREK2, (2) SF rate and Em, and (3) spontaneous pain behavior and C-nociceptor SF rate suggested that TREK2 knockdown might increase spontaneous pain. After CFA-induced inflammation, spontaneous foot lifting (a measure of spontaneous pain) was (1) greater in rats with naturally lower TREK2 in ipsilateral small DRG neurons and (2) increased by siRNA-induced TREK2 knockdown in vivo. We conclude that TREK2 hyperpolarizes IB4 binding C-nociceptors and limits pathological spontaneous pain. Similar TREK2 distributions in small DRG neurons of several species suggest that these role(s) of TREK2 may be widespread.

Published
2014

48. Association of Interleukin-6 and Other Cytokines with Self-Reported Pain in Prostate Cancer Patients Receiving Chemotherapy.

Author

Al-Mazidi, Sarah, Farhat, Karim, Nedjadi, TaoufiK, Chaudhary, Adeel, Al-Abdin, Osman Zin, Rabah, Danny, Al-Zoghaibi, Mohammad, and Djouhri, Laiche

Subjects
PROSTATE tumors, BIOLOGICAL assay, CANCER chemotherapy, CANCER patients, INTERLEUKINS, METASTASIS, PALLIATIVE treatment, REPORT writing, HEALTH self-care, CONTROL groups, RETROSPECTIVE studies, DATA analysis software, KRUSKAL-Wallis Test, DIAGNOSIS
Abstract

Background. Pain is a common and dose-limiting side effect of many potentially curative cancer chemotherapeutic agents. This chemotherapy-induced pain (CIP) affects the quality of life of cancer patients and survivors and hampers the optimal clinical management of chemotherapy in cancer patients. The underlying mechanisms remain largely unknown, but changes in levels of cytokines/chemokines may contribute to the pathophysiology of CIP. Objective. This retrospective study was aimed at examining whether plasma levels of various cytokines change in prostate cancer patients after chemotherapy treatment and whether such changes (if any) are associated with their pain intensity. Methods. Using a Luminex assay, plasma levels of 27 cytokines/chemokines were measured in 78 men: 30 patients with metastatic prostate cancer who received chemotherapy (Docetaxel, 75mg/m2 intravenously), 29 untreated patients with nonmetastatic prostate cancer, and 19 healthy controls. Subjective pain was assessed in chemotherapytreated cancer patients using the 11-point numeric rating scale (NRS) pain scores. Results. Chemotherapy-treated patients with pain (NRS≥3) exhibited significantly increased levels of the pro-inflammatory cytokines (IL-6, IL-8) and chemokines (Eotaxin, VEGF, and IP-10) compared with untreated cancer patients or with patients without pain (NRS=0). Of the 27 cytokines examined, only IL-6 was positively correlated with pain intensity in the chemotherapy-treated patients with pain. Conclusions. These findings suggest that the cytokines, particularly IL-6, whose levels were elevated in the chemotherapy-treated patients may be involved in the pathophysiology of CIP, and that they might be potential new targets for pain control in cancer patients receiving chemotherapy. [ABSTRACT FROM AUTHOR]

Published
2018
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