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7. The toll like receptor 7 pathway and the sex bias of systemic lupus erythematosus.

Author

Scofield, R. Hal, Wren, Jonathan D., and Lewis, Valerie M.

Abstract

Systemic lupus erythematosus (SLE) predominately affects women with a ratio of females-to-males of about 9:1. The complement of sex chromosomes may play and important role in the mechanism of the sex bias. Previous work has shown that men with Klinefleter's syndrome (47,XXY) as well as women with 47,XXX are found in excess among SLE patients well as among Sjogren's disease, systemic sclerosis and idiopathic inflammatory myositis. in cells with more than one X chromosome, all but one is inactivated. However, X chromosome inactivation, as mediated by the long noncoding RNA X-inactive specific transcript, or XIST, is not complete with approximately 10% of genes in the non-recombining region of the X chromosome escaping X inactivation. In the TLR7 signaling pathway, both the TLR7 and TLR adaptor interacting with endolysosomal SLC15A4 (TASL) escape X inactivation. Comparing male and female immune cells, there is increased TLR7 signaling related to increased expression of these genes in cells with more than one X chromosome. Cells with more than one X chromosome also express XIST, while cells with one X chromosome do not. XIST, as a source of ligand for TLR7, has also been shown to increase TLR7 signaling. Thus, we propose that both these mechanisms operating in immune cells with more than one X chromosome may act in a mutual way to mediate an X chromosome dose effect for the sex bias of autoimmune disease. [ABSTRACT FROM AUTHOR]

Published
2025
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11. Biallelic variants in KARS1 are associated with neurodevelopmental disorders and hearing loss recapitulated by the knockout zebrafish

Author

Lin, Sheng-Jia, Vona, Barbara, Barbalho, Patricia G., Kaiyrzhanov, Rauan, Maroofian, Reza, Petree, Cassidy, Severino, Mariasavina, Stanley, Valentina, Varshney, Pratishtha, Bahena, Paulina, Alzahrani, Fatema, Alhashem, Amal, Pagnamenta, Alistair T., Aubertin, Gudrun, Estrada-Veras, Juvianee I., Hernández, Héctor Adrián Díaz, Mazaheri, Neda, Oza, Andrea, Thies, Jenny, Renaud, Deborah L., Dugad, Sanmati, McEvoy, Jennifer, Sultan, Tipu, Pais, Lynn S., Tabarki, Brahim, Villalobos-Ramirez, Daniel, Rad, Aboulfazl, Ambrose, J.C., Arumugam, P., Bleda, M., Boardman-Pretty, F., Boustred, C.R., Brittain, H., Caulfield, M.J., Chan, G.C., Fowler, T., Giess, A., Hamblin, A., Henderson, S., Hubbard, T.J.P., Jackson, R., Jones, L.J., Kasperaviciute, D., Kayikci, M., Kousathanas, A., Lahnstein, L., Leigh, S.E.A., Leong, I.U.S., Lopez, F.J., Maleady-Crowe, F., Moutsianas, L., Mueller, M., Murugaesu, N., Need, A.C., O‘Donovan, P., Odhams, C.A., Patch, C., Perez-Gil, D., Pereira, M.B., Pullinger, J., Rahim, T., Rendon, A., Rogers, T., Savage, K., Sawant, K., Scott, R.H., Siddiq, A., Sieghart, A., Smith, S.C., Sosinsky, A., Stuckey, A., Tanguy, M., Thomas, E.R.A., Thompson, S.R., Tucci, A., Walsh, E., Welland, M.J., Williams, E., Witkowska, K., Wood, S.M., Galehdari, Hamid, Ashrafzadeh, Farah, Sahebzamani, Afsaneh, Saeidi, Kolsoum, Torti, Erin, Elloumi, Houda Z., Mora, Sara, Palculict, Timothy B., Yang, Hui, Wren, Jonathan D., Ben Fowler, Joshi, Manali, Behra, Martine, Burgess, Shawn M., Nath, Swapan K., Hanna, Michael G., Kenna, Margaret, Merritt, J. Lawrence, II, Houlden, Henry, Karimiani, Ehsan Ghayoor, Zaki, Maha S., Haaf, Thomas, Alkuraya, Fowzan S., Gleeson, Joseph G., and Varshney, Gaurav K.

Published
2021
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15. Identification of susceptibility loci for Takayasu arteritis through a large multi-ancestral genome-wide association study

Author

Ortiz-Fernández, Lourdes, Saruhan-Direskeneli, Güher, Alibaz-Oner, Fatma, Kaymaz-Tahra, Sema, Coit, Patrick, Kong, Xiufang, Kiprianos, Allan P., Maughan, Robert T., Aydin, Sibel Z., Aksu, Kenan, Keser, Gokhan, Kamali, Sevil, Inanc, Murat, Springer, Jason, Akar, Servet, Onen, Fatos, Akkoc, Nurullah, Khalidi, Nader A., Koening, Curry, Karadag, Omer, Kiraz, Sedat, Forbess, Lindsy, Langford, Carol A., McAlear, Carol A., Ozbalkan, Zeynep, Yavuz, Sule, Çetin, Gozde Yildirim, Alpay-Kanitez, Nilufer, Chung, Sharon, Ates, Askin, Karaaslan, Yasar, McKinnon-Maksimowicz, Kathleen, Monach, Paul A., Ozer, Hüseyin T.E., Seyahi, Emire, Fresko, Izzet, Cefle, Ayse, Seo, Philip, Warrington, Kenneth J., Ozturk, Mehmet A., Ytterberg, Steven R., Cobankara, Veli, Onat, Ahmet Mesut, Duzgun, Nurşen, Bıcakcıgil, Muge, Yentür, Sibel P., Lally, Lindsay, Manfredi, Angelo A., Baldissera, Elena, Erken, Eren, Yazici, Ayten, Kısacık, Bünyamin, Kaşifoğlu, Timuçin, Dalkilic, Ediz, Cuthbertson, David, Pagnoux, Christian, Sreih, Antoine, Reales, Guillermo, Wallace, Chris, Wren, Jonathan D., Cunninghame-Graham, Deborah S., Vyse, Timothy J., Sun, Ying, Chen, Huiyong, Grayson, Peter C., Tombetti, Enrico, Jiang, Lindi, Mason, Justin C., Merkel, Peter A., Direskeneli, Haner, and Sawalha, Amr H.

Published
2021
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16. The nitrone compound OKN-007 delays motor neuron loss and disease progression in the G93A mouse model of amyotrophic lateral sclerosis.

Author

Bhaskaran, Shylesh, Piekarz, Katarzyna M., Brown, Jacob, Yang, Brian, Ocañas, Sarah R., Wren, Jonathan D., Georgescu, Constantin, Bottoms, Christopher, Murphy, Ashley, Thomason, Jessica, Saunders, Debra, Smith, Nataliya, Towner, Rheal, and Van Remmen, Holly

Subjects
AMYOTROPHIC lateral sclerosis, MOTOR neuron diseases, SPINAL cord diseases, SPINAL cord, MUSCULAR atrophy
Abstract

Our study investigated the therapeutic potential of OKN-007 in the SOD1 G93A mouse model of amyotrophic lateral sclerosis (ALS). The impact of OKN-007, known for its antioxidant, anti-inflammatory, and neuroprotective properties, was tested at two doses (150 mg/kg and 300 mg/kg) at onset and late-stage disease. Results demonstrated a significant delay in disease progression at both doses, with treated mice showing a slower advance to early disease stages compared to untreated controls. Motor neuron counts in the lumbar spinal cord were notably higher in OKN-007 treated mice at the time of disease onset, suggesting neuroprotection. Additionally, OKN-007 reduced microglial activation and preserved reduced neuromuscular junction fragmentation, although it did not significantly alter the increase in astrocyte number or the decline in hindlimb muscle mass. MR spectroscopy (MRS) revealed improved spinal cord perfusion and normalized myo-inositol levels in treated mice, supporting reduced neuroinflammation. While the expression of several proteins associated with inflammation is increased in spinal cord extracts from G93A mice, OKN-007 dampened the expression of IL-1β, IL-1ra and IL-1α. Despite its promising effects on early-stage disease progression, in general, the beneficial effects of OKN-007 diminished over longer treatment durations. Further, we found no improvement in muscle atrophy or weakness phenotypes in OKN-007 treated G93A mice, and no effect on mitochondrial function or lifespan. Overall, our findings suggest that OKN-007 holds potential as a disease-modifying treatment for ALS, although further research is needed to optimize dosing regimens and understand its long-term effects. [ABSTRACT FROM AUTHOR]

Published
2024
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17. Unacylated Ghrelin Protects Against Age‐Related Loss of Muscle Mass and Contractile Dysfunction in Skeletal Muscle.

Author

Kim, Hyunyoung, Ranjit, Rojina, Claflin, Dennis R., Georgescu, Constantin, Wren, Jonathan D., Brooks, Susan V., Miller, Benjamin F., and Ahn, Bumsoo

Subjects
GHRELIN receptors, MUSCULAR atrophy, MYONEURAL junction, QUADRICEPS muscle, SKELETAL muscle, MUSCLE mass, SARCOPENIA
Abstract

Sarcopenia, the progressive loss of muscle mass and function, universally affects older adults and is closely associated with frailty and reduced quality of life. Despite the inevitable consequences of sarcopenia and its relevance to healthspan, no pharmacological therapies are currently available. Ghrelin is a gut‐released hormone that increases appetite and body weight through acylation. Acylated ghrelin activates its receptor, growth hormone secretagogue receptor 1a (GHSR1a), in the brain by binding to it. Studies have demonstrated that acyl and unacylated ghrelin (UnAG) both have protective effects against acute pathological conditions independent of receptor activation. Here, we investigated the long‐term effects of UnAG in age‐associated muscle atrophy and contractile dysfunction in mice. Four‐month‐old and 18‐month‐old mice were subjected to either UnAG or control treatment for 10 months. UnAG did not affect food consumption or body weight. Gastrocnemius and quadriceps muscle weights were reduced by 20%–30% with age, which was partially protected against by UnAG. Specific force, force per cross‐sectional area, measured in isolated extensor digitorum longus muscle was diminished by 30% in old mice; however, UnAG prevented the loss of specific force. UnAG also protected from decreases in mitochondrial respiration and increases in hydrogen peroxide generation of skeletal muscle of old mice. Results of bulk mRNA‐seq analysis and our contractile function data show that UnAG reversed neuromuscular junction impairment that occurs with age. Collectively, our data revealed the direct role of UnAG in mitigating sarcopenia in mice, independent of food consumption or body weight, implicating UnAG treatment as a potential therapy against sarcopenia. [ABSTRACT FROM AUTHOR]

Published
2024
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20. CD151 Maintains Endolysosomal Protein Quality to Inhibit Vascular Inflammation

Author

Chen, Junxiong, primary, Ding, Yingjun, additional, Jiang, Chao, additional, Qu, Rongmei, additional, Wren, Jonathan D., additional, Georgescu, Constantin, additional, Wang, Xuejun, additional, Reuter, Darlene N., additional, Liu, Beibei, additional, Giles, Cory B., additional, Mayr, Christoph H., additional, Schiller, Herbert B., additional, Dai, Jingxing, additional, Stipp, Christopher S., additional, Subramaniyan, Bharathiraja, additional, Wang, Jie, additional, Zuo, Houjuan, additional, Huang, Chao, additional, Fung, Kar-Ming, additional, Rice, Heather C., additional, Sonnenberg, Arnoud, additional, Wu, David, additional, Walters, Matthew S., additional, Zhao, You-Yang, additional, Kanie, Tomoharu, additional, Hays, Franklin A., additional, Papin, James F., additional, Wang, Dao Wen, additional, and Zhang, Xin A., additional

Published
2024
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22. Fragmentstein—facilitating data reuse for cell-free DNA fragment analysis

Author

Wren, Jonathan, Wren, J ( Jonathan ), Balázs, Zsolt; https://orcid.org/0000-0003-3537-7441, Gitchev, Todor; https://orcid.org/0000-0002-7470-0646, Ivanković, Ivna, Krauthammer, Michael, Wren, Jonathan, Wren, J ( Jonathan ), Balázs, Zsolt; https://orcid.org/0000-0003-3537-7441, Gitchev, Todor; https://orcid.org/0000-0002-7470-0646, Ivanković, Ivna, and Krauthammer, Michael

Abstract

Method development for the analysis of cell-free DNA (cfDNA) sequencing data is impeded by limited data sharing due to the strict control of sensitive genomic data. An existing solution for facilitating data sharing removes nucleotide-level information from raw cfDNA sequencing data, keeping alignment coordinates only. This simplified format can be publicly shared and would, theoretically, suffice for common functional analyses of cfDNA data. However, current bioinformatics software requires nucleotide-level information and cannot process the simplified format. We present Fragmentstein, a command-line tool for converting non-sensitive cfDNA-fragmentation data into alignment mapping (BAM) files. Fragmentstein complements fragment coordinates with sequence information from a reference genome to reconstruct BAM files. We demonstrate the utility of Fragmentstein by showing the feasibility of copy number variant (CNV), nucleosome occupancy, and fragment length analyses from non-sensitive fragmentation data. Availability and implementatio: Implemented in bash, Fragmentstein is available at https://github.com/uzh-dqbm-cmi/fragmentstein, licensed under GNU GPLv3.

Published
2024

25. Circulating anti-geronic factors from heterochonic parabionts promote vascular rejuvenation in aged mice: transcriptional footprint of mitochondrial protection, attenuation of oxidative stress, and rescue of endothelial function by young blood

Author

Kiss, Tamas, Tarantini, Stefano, Csipo, Tamas, Balasubramanian, Priya, Nyúl-Tóth, Ádám, Yabluchanskiy, Andriy, Wren, Jonathan D., Garman, Lori, Huffman, Derek M., Csiszar, Anna, and Ungvari, Zoltan

Published
2020
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29. Dynamics of microRNA secreted via extracellular vesicles during the maturation of embryonic stem cell‐derived retinal pigment epithelium.

Author

Pollalis, Dimitrios, Nair, Gopa Kumar Gopinadhan, Leung, Justin, Bloemhof, Clarisa Marie, Bailey, Jeffrey K., Pennington, Britney O., Kelly, Kaitlin R., Khan, Amir I., Yeh, Ashley K., Sundaram, Kartik S., Clegg, Dennis O., Peng, Chen‐Ching, Xu, Liya, Georgescu, Constantin, Wren, Jonathan D., and Lee, Sun Young

Subjects
HUMAN embryonic stem cells, PLURIPOTENT stem cells, RHODOPSIN, EXTRACELLULAR vesicles, PARACRINE mechanisms
Abstract

Retinal pigment epithelial (RPE) cells are exclusive to the retina, critically multifunctional in maintaining the visual functions and health of photoreceptors and the retina. Despite their vital functions throughout lifetime, RPE cells lack regenerative capacity, rendering them vulnerable which can lead to degenerative retinal diseases. With advancements in stem cell technology enabling the differentiation of functional cells from pluripotent stem cells and leveraging the robust autocrine and paracrine functions of RPE cells, extracellular vesicles (EVs) secreted by RPE cells hold significant therapeutic potential in supplementing RPE cell activity. While previous research has primarily focused on the trophic factors secreted by RPE cells, there is a lack of studies investigating miRNA, which serves as a master regulator of gene expression. Profiling and defining the functional role of miRNA contained within RPE‐secreted EVs is critical as it constitutes a necessary step in identifying the optimal phenotype of the EV‐secreting cell and understanding the biological cargo of EVs to develop EV‐based therapeutics. In this study, we present a comprehensive profile of miRNA in small extracellular vesicles (sEVs) secreted during RPE maturation following differentiation from human embryonic stem cells (hESCs); early‐stage hESC‐RPE (20–21 days in culture), mid‐stage hESC‐RPE (30–31 days in culture) and late‐stage hESC‐RPE (60–61 days in culture). This exploration is essential for ongoing efforts to develop and optimize EV‐based intraocular therapeutics utilizing RPE‐secreted EVs, which may significantly impact the function of dysfunctional RPE cells in retinal diseases. [ABSTRACT FROM AUTHOR]

Published
2024
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43. Fig. S7 from Absence of Either Ripk3 or Mlkl Reduces Incidence of Hepatocellular Carcinoma Independent of Liver Fibrosis

Author

Mohammed, Sabira, primary, Thadathil, Nidheesh, primary, Ohene-Marfo, Phoebe, primary, Tran, Albert L., primary, Van Der Veldt, Michael, primary, Georgescu, Constantin, primary, Oh, Sangphil, primary, Nicklas, Evan H., primary, Wang, Dawei, primary, Haritha, Nair Hariprasad, primary, Luo, Wenyi, primary, Janknecht, Ralf, primary, Miller, Benjamin F., primary, Wren, Jonathan D., primary, Freeman, Willard M., primary, and Deepa, Sathyaseelan S., primary

Published
2023
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44. Supplementary Table 1 from Absence of Either Ripk3 or Mlkl Reduces Incidence of Hepatocellular Carcinoma Independent of Liver Fibrosis

Author

Mohammed, Sabira, primary, Thadathil, Nidheesh, primary, Ohene-Marfo, Phoebe, primary, Tran, Albert L., primary, Van Der Veldt, Michael, primary, Georgescu, Constantin, primary, Oh, Sangphil, primary, Nicklas, Evan H., primary, Wang, Dawei, primary, Haritha, Nair Hariprasad, primary, Luo, Wenyi, primary, Janknecht, Ralf, primary, Miller, Benjamin F., primary, Wren, Jonathan D., primary, Freeman, Willard M., primary, and Deepa, Sathyaseelan S., primary

Published
2023
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45. Supplementary Table 2 from Absence of Either Ripk3 or Mlkl Reduces Incidence of Hepatocellular Carcinoma Independent of Liver Fibrosis

Author

Mohammed, Sabira, primary, Thadathil, Nidheesh, primary, Ohene-Marfo, Phoebe, primary, Tran, Albert L., primary, Van Der Veldt, Michael, primary, Georgescu, Constantin, primary, Oh, Sangphil, primary, Nicklas, Evan H., primary, Wang, Dawei, primary, Haritha, Nair Hariprasad, primary, Luo, Wenyi, primary, Janknecht, Ralf, primary, Miller, Benjamin F., primary, Wren, Jonathan D., primary, Freeman, Willard M., primary, and Deepa, Sathyaseelan S., primary

Published
2023
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46. Data from Absence of Either Ripk3 or Mlkl Reduces Incidence of Hepatocellular Carcinoma Independent of Liver Fibrosis

Author

Mohammed, Sabira, primary, Thadathil, Nidheesh, primary, Ohene-Marfo, Phoebe, primary, Tran, Albert L., primary, Van Der Veldt, Michael, primary, Georgescu, Constantin, primary, Oh, Sangphil, primary, Nicklas, Evan H., primary, Wang, Dawei, primary, Haritha, Nair Hariprasad, primary, Luo, Wenyi, primary, Janknecht, Ralf, primary, Miller, Benjamin F., primary, Wren, Jonathan D., primary, Freeman, Willard M., primary, and Deepa, Sathyaseelan S., primary

Published
2023
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47. Supplementary Data Legends from Absence of Either Ripk3 or Mlkl Reduces Incidence of Hepatocellular Carcinoma Independent of Liver Fibrosis

Author

Mohammed, Sabira, primary, Thadathil, Nidheesh, primary, Ohene-Marfo, Phoebe, primary, Tran, Albert L., primary, Van Der Veldt, Michael, primary, Georgescu, Constantin, primary, Oh, Sangphil, primary, Nicklas, Evan H., primary, Wang, Dawei, primary, Haritha, Nair Hariprasad, primary, Luo, Wenyi, primary, Janknecht, Ralf, primary, Miller, Benjamin F., primary, Wren, Jonathan D., primary, Freeman, Willard M., primary, and Deepa, Sathyaseelan S., primary

Published
2023
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48. Supplementary Table 3 from Absence of Either Ripk3 or Mlkl Reduces Incidence of Hepatocellular Carcinoma Independent of Liver Fibrosis

Author

Mohammed, Sabira, primary, Thadathil, Nidheesh, primary, Ohene-Marfo, Phoebe, primary, Tran, Albert L., primary, Van Der Veldt, Michael, primary, Georgescu, Constantin, primary, Oh, Sangphil, primary, Nicklas, Evan H., primary, Wang, Dawei, primary, Haritha, Nair Hariprasad, primary, Luo, Wenyi, primary, Janknecht, Ralf, primary, Miller, Benjamin F., primary, Wren, Jonathan D., primary, Freeman, Willard M., primary, and Deepa, Sathyaseelan S., primary

Published
2023
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