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101. Myeloid-specific deletion of Zfp36 protects against insulin resistance and fatty liver in diet-induced obese mice

Author

Caracciolo, Valentina, primary, Young, Jeanette, additional, Gonzales, Donna, additional, Ni, Yingchun, additional, Flowers, Stephen J., additional, Summer, Ross, additional, Waldman, Scott A., additional, Kim, Jason K., additional, Jung, Dae Young, additional, Noh, Hye Lim, additional, Kim, Taekyoon, additional, Blackshear, Perry J., additional, O'Connell, Danielle, additional, Bauer, Robert C., additional, and Kallen, Caleb B., additional

Published
2018
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103. Proteomic Profile of TGF-β1 treated Lung Fibroblasts identifies Novel Markers of Activated Fibroblasts in the Silica Exposed Rat Lung

Author

Na, Mao, primary, Hong, Xu, additional, Fuyu, Jin, additional, Dingjie, Xu, additional, Sales, Dominic, additional, Hui, Zhang, additional, Zhongqiu, Wei, additional, Shifeng, Li, additional, Xuemin, Gao, additional, Wenchen, Cai, additional, Dan, Li, additional, Guizhen, Zhang, additional, Bonan, Zhang, additional, Lijuan, Zhang, additional, Shumin, Li, additional, Ying, Zhu, additional, Jin, Wang, additional, Mingwang, Rui, additional, Summer, Ross, additional, and Fang, Yang, additional

Published
2018
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104. Lipid Synthesis Is Required to Resolve Endoplasmic Reticulum Stress and Limit Fibrotic Responses in the Lung

Author

Romero, Freddy, primary, Hong, Xu, additional, Shah, Dilip, additional, Kallen, Caleb B., additional, Rosas, Ivan, additional, Guo, Zhi, additional, Schriner, DeLeila, additional, Barta, Julie, additional, Shaghaghi, Hoora, additional, Hoek, Jan B., additional, Mesaros, Clementina, additional, Choi, Augustine M., additional, Snyder, Nathaniel W., additional, and Summer, Ross, additional

Published
2018
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106. Reclaiming the Balance: Blocking Glutamine Uptake to Restrain Pulmonary Fibrosis.

Author

Gang Liu and Summer, Ross

Subjects
PULMONARY fibrosis, GLUTAMINE, MOLECULAR biology, MOLECULAR volume, STUDENTS
Abstract

An editorial is presented on a novel approach to treat pulmonary fibrosis by targeting glutamine uptake, a process essential for the function and growth of myofibroblasts. Topics include the role of myofibroblasts in lung fibrosis, the dependency of myofibroblasts on glutamine for essential functions, and the promising therapeutic potential of blocking glutamine uptake through Solute Carrier Family 1 Member 5 (SLC1A5) inhibition in the treatment of pulmonary fibrosis.

Published
2023
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112. An Official American Thoracic Society Workshop Report: Obesity and Metabolism. An Emerging Frontier in Lung Health and Disease

Author

Suratt, Benjamin T., primary, Ubags, Niki D. J., additional, Rastogi, Deepa, additional, Tantisira, Kelan G., additional, Marsland, Benjamin J., additional, Petrache, Irina, additional, Allen, Janice B., additional, Bates, Jason H. T., additional, Holguin, Fernando, additional, McCormack, Meredith C., additional, Michelakis, Evangelos D., additional, Black, Stephen M., additional, Jain, Manu, additional, Mora, Ana L., additional, Natarajan, Viswanathan, additional, Miller, Yury I., additional, Fessler, Michael B., additional, Birukov, Konstantin G., additional, Summer, Ross S., additional, Shore, Stephanie A., additional, and Dixon, Anne E., additional

Published
2017
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114. Obesity-induced adipokine imbalance impairs mouse pulmonary vascular endothelial function and primes the lung for injury

Author

Shah, Dilip, Romero, Freddy, Duong, Michelle, Wang, Nadan, Paudyal, Bishnuhari, Suratt, Benjamin T., Kallen, Caleb B., Sun, Jianxin, Zhu, Ying, Walsh, Kenneth, and Summer, Ross

Subjects
Article
Abstract

Obesity is a risk factor for the development of acute respiratory distress syndrome (ARDS) but mechanisms mediating this association are unknown. While obesity is known to impair systemic blood vessel function, and predisposes to systemic vascular diseases, its effects on the pulmonary circulation are largely unknown. We hypothesized that the chronic low grade inflammation of obesity impairs pulmonary vascular homeostasis and primes the lung for acute injury. The lung endothelium from obese mice expressed higher levels of leukocyte adhesion markers and lower levels of cell-cell junctional proteins when compared to lean mice. We tested whether systemic factors are responsible for these alterations in the pulmonary endothelium; treatment of primary lung endothelial cells with obese serum enhanced the expression of adhesion proteins and reduced the expression of endothelial junctional proteins when compared to lean serum. Alterations in pulmonary endothelial cells observed in obese mice were associated with enhanced susceptibility to LPS-induced lung injury. Restoring serum adiponectin levels reversed the effects of obesity on the lung endothelium and attenuated susceptibility to acute injury. Our work indicates that obesity impairs pulmonary vascular homeostasis and enhances susceptibility to acute injury and provides mechanistic insight into the increased prevalence of ARDS in obese humans.

Published
2015

115. T-cadherin deficiency increases vascular vulnerability in T2DM through impaired NO bioactivity.

Author

Wang, Han, Tao, Ling, Ambrosio, Anastasia, Yan, Wenjun, Summer, Ross, Lau, Wayne Bond, Wang, Yajing, Ma, Xin-Liang, Wang, Han, Tao, Ling, Ambrosio, Anastasia, Yan, Wenjun, Summer, Ross, Lau, Wayne Bond, Wang, Yajing, and Ma, Xin-Liang

Abstract

BACKGROUND: Endothelial dysfunction plays a critical role in the development of type 2 diabetes (T2DM). T-cadherin (T-cad) has gained recognition as a regulator of endothelial cell (EC) function. The present study examined whether T-cad deficiency increases vascular vulnerability in T2DM. METHODS: Vascular segments were isolated from WT or T-cad knockout mice. Endothelial function, total NO accumulation, and the expression of T-cad related proteins were determined. RESULTS: Ach and acidified NaNO2 induced similar vasorelaxation in WT groups. T-cad KO mice exhibited normal response to acidified NaNO2, but manifested markedly reduced response to Ach. NO accumulation was also decreased in T-cad KO group. T-cad expression was reduced in WT mice fed 8 weeks of high fat diet (HFD). Furthermore, exacerbated reduction of vasorelaxation was observed in T-cad KO mice fed 8 weeks of HFD. CONCLUSIONS: In the current study, we provide the first in vivo evidence that T-cadherin deficiency causes endothelial dysfunction in T2DM vascular segments, suggesting the involvement of T-cad deficiency in T2DM pathogenesis.

Published
2017

118. Fine-tuning the ubiquitin-proteasome system to treat pulmonary fibrosis.

Author

Roque, Willy, Summer, Ross, and Romero, Freddy

Subjects
*UBIQUITINATION, *PULMONARY fibrosis treatment, *LUNG diseases, *COLLAGEN, *PROTEOLYSIS
Abstract

Idiopathic pulmonary fibrosis (IPF) is an extremely aggressive lung disease that develops almost exclusively in older individuals, carries a very poor prognosis, and lacks any truly effective therapies. The current conceptual model is that IPF develops because of an age-related decline in the ability of the lung epithelium to regenerate after injury, largely due to death or senescence of epithelial progenitor cells in the distal airways. This loss of regenerative capacity is thought to initiate a chronic and ineffective wound-healing response, characterized by persistent, low-grade lung inflammation and sustained production of collagen and other extracellular matrix materials. Despite recent advances in our understanding of IPF pathobiology, there remains a pressing need to further delineate underlying mechanisms to develop more effective therapies for this disease. In this review, we build the case that many of the manifestations of IPF result from a failure of cells to effectively manage their proteome. We propose that epithelial progenitor cells, as well as immune cells and fibroblasts, become functionally impaired, at least in part, because of an accumulation or a loss in the expression of various crucial proteins. Further, we propose that central to this defect is the dysregulation of the ubiquitin-proteasome system (UPS), which is the major protein-degradation system in eukaryotic cells. Lastly, borrowing concepts from other fields, we discuss how targeting the UPS system could be employed as a novel treatment for IPF and perhaps for other fibrotic lung diseases as well. [ABSTRACT FROM AUTHOR]

Published
2019
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119. Scleroderma Related Lung Disease: Is There a Pathogenic Role for Adipokines?

Author

Haley, Shannon, Shah, Dilip, Romero, Freddy, and Summer, Ross

Subjects
Leptin, Scleroderma, Systemic, Adipokines, Hypertension, Pulmonary, Humans, Adiponectin, Lung Diseases, Interstitial, Article
Abstract

Scleroderma is a systemic autoimmune disease of unknown etiology whose characteristic features include endothelial cell dysfunction, fibroblast proliferation, and immune dysregulation. Although almost any organ can be pathologically involved in scleroderma, lung complications including interstitial lung disease (ILD) and pulmonary arterial hypertension (PAH) are the leading cause of death in patients with this condition. Currently, the molecular mechanisms leading to development of scleroderma-related lung disease are poorly understood; however, the systemic nature of this condition has led many to implicate circulating factors in the pathogenesis of some of its organ impairment. In this article we focus on a new class of circulating factors derived from adipose-tissue called adipokines, which are known to be altered in scleroderma. Recently, the adipokines adiponectin and leptin have been found to regulate biological activity in endothelial, fibroblast, and immune cell types in lung and in many other tissues. The pleiotropic nature of these circulating factors and their functional activity on many cell types implicated in the pathogenesis of ILD and PAH suggest these hormones may be mechanistically involved in the onset and/or progression of scleroderma-related lung diseases.

Published
2013

120. Pulmonary Circulation in Obesity, Diabetes, and Metabolic Syndrome

Author

Khaing, Phue, Pandit, Pooja, Awsare, Bharat, and Summer, Ross

Abstract

Obesity, diabetes mellitus, and the metabolic syndrome are important risk factors for the development of cardiovascular disease, with significant impact on human morbidity and mortality. Several decades of research have accumulated considerable knowledge about the mechanisms by which metabolic conditions precipitate systemic cardiovascular diseases. In short, these mechanisms are thought to involve changes in the external environment of vascular cells, which are mediated by the pro-inflammatory effects of adipokines, free fatty acids, and hyperglycemia. Thus, it has been hypothesized that the pulmonary circulation, witnessing similar insults as the systemic circulation, may be equally vulnerable to the development of vascular disease. Accordingly, recent attention has focused on exploring the mechanistic and epidemiological relationships among obesity, type 2 diabetes mellitus, metabolic syndrome, and pulmonary vascular diseases. In this article, we discuss in detail the preclinical evidence showing a modest but perceivable impact of metabolic disorders on the pulmonary circulation. In addition, we review the existing epidemiological studies examining the relationship among cardiovascular risk factors and pulmonary vascular diseases, using the acute respiratory distress syndrome and pulmonary arterial hypertension as examples. We conclude by discussing areas of limitations in the field and by suggesting future directions for investigation, including the notion that the pulmonary circulation may, in fact, be a resilient entity in the setting of some metabolic perturbations. © 2020 American Physiological Society. Compr Physiol10:297-316, 2020. P. Khaing, P. Pandit, B. Awsare, R. Summer.Pulmonary Circulation in Obesity, Diabetes, and Metabolic Syndrome. Compr Physiol10: 2020, 297-316. Obesity and type 2 diabetes mellitus (T2DM) are major risk factors for the development and progression of systemic cardiovascular diseases.The pulmonary circulation receives comparable exposures as the systemic circulation, yet the pulmonary circulation is mostly immune from developing atherosclerotic diseases.The effects of obesity and T2DM on the pulmonary circulation vary depending on the type of experimental models employed.An accepted gold-standard preclinical model for obesity or T2DM does not exist.Human studies suggest that obesity increases susceptibility for ARDS but reduces its overall mortality.WHO groups 2 and 3 are the most common causes of pulmonary hypertension in individuals with obesity and T2DM.Obesity, T2DM, and the metabolic syndrome have a modest but observable impact on the pulmonary circulation, but overall findings suggest that the pulmonary vasculature may be a resilient entity to metabolic exposures. The following legends to the figures that appear throughout the article are written to be useful for teaching. Figure 1 Teaching points: Adipose tissue adopts a dysfunctional phenotype in the obese state, releasing higher concentrations of pro-inflammatory adipokines and free fatty acids into the circulation, which then impart deleterious effects on systemic blood vessels by inducing inflammation and oxidative stress. Figure 2 Teaching points: Insulin resistance in type 2 diabetes mellitus is associated with elevated blood glucose levels (i.e., hyperglycemia). As a result, high levels of intracellular glucose lead to cellular injury of endothelial cells via several mechanisms, including increased production of sorbitol, formation of advanced glycation end products (AGEs), and activation of protein kinase C (PKC). Figure 3 Teaching points: The acute respiratory distress syndrome (ARDS) is a life-threatening lung disease that can develop as a result of direct pulmonary injury (e.g., pneumonia) or in association with extrapulmonary illnesses (e.g., sepsis, pancreatitis, and major trauma). An aberrant inflammatory response that disrupts epithelial and endothelial barrier protection in the lung is thought to be a key mechanism in ARDS pathophysiology. Figure 4 Teaching points: Pulmonary arterial hypertension (PAH) is caused by progressive histological changes, which lead to irreversible remodeling of pulmonary blood vessels. These changes are associated with perivascular infiltration of immune cells, chronic development of vascular leakage, and production of inflammatory mediators. These mechanisms cause endothelial dysfunction and contribute to the hyperproliferative and antiapoptotic phenotype characteristic of endothelial cells in PAH.

Published
2020
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123. Binding of CIB1 to the αIIb tail of αIIbβ3 is required for FAK recruitment and activation in platelets.

Author

Naik, Meghna U., Naik, Tejal U., Summer, Ross, and Naik, Ulhas P.

Subjects
FOCAL adhesion kinase, BLOOD platelets, CELL membranes, FIBRINOGEN, CYTOSKELETON
Abstract

Background: It is believed that activation of c-Src bound to the integrin β3 subunit initiates outside-in signaling. The involvement of αIIb in outside-in signaling is poorly understood. Objectives: We have previously shown that CIB1 specifically interacts with the cytoplasmic domain of αIIb and is required for αIIbβ3 outside-in signaling. Here we evaluated the role of CIB1 in regulating outside-in signaling in the absence of inside-out signaling. Methods: We used αIIb cytoplasmic domain peptide and CIB1-function blocking antibody to inhibit interaction of CIB1 with αIIb subunit as well as Cib1-/- platelets to evaluate the consequence of CIB1 interaction with αIIb on outside-in signaling. Results: Fibrinogen binding to αIIbβ3 results in calcium-dependent interaction of CIB1 with αIIb, which is not required for filopodia formation. Dynamic rearrangement of cytoskeleton results in CIB1-dependent recruitment of FAK to the αIIb complex and its activation. Disruption of the association of CIB1 and αIIb by incorporation of αIIb peptide or anti-CIB1 inhibited both FAK association and activation. Furthermore, FAK recruitment to the integrin complex was required for c-Src activation. Inhibition of c-Src had no effect on CIB1 accumulation with the integrin at the filopodia, suggesting that c-Src activity is not required for the formation of CIB1-αIIb-FAK complex. Conclusion: Our results suggest that interaction of CIB1 with αIIb is one of the early events occurring during outside-in signaling. Furthermore, CIB1 recruits FAK to the αIIbβ3 complex at the filopodia where FAK is activated, which in turn activates c-Src, resulting in propagation of outside-in signaling leading to platelet spreading. [ABSTRACT FROM AUTHOR]

Published
2017
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126. Acute respiratory distress syndrome: epidemiology and management approaches

Author

Walkey,Allan J, Summer,Ross, Ho,Vu, Alkana,Philip, Walkey,Allan J, Summer,Ross, Ho,Vu, and Alkana,Philip

Abstract

Allan J Walkey,1 Ross Summer,1 Vu Ho,1 Philip Alkana21The Pulmonary Center, Boston University School of Medicine, Boston, MA, USA; 2Asthma Research Center, Brigham and Women's Hospital, Boston, MA, USAAbstract: Acute lung injury and the more severe acute respiratory distress syndrome represent a spectrum of lung disease characterized by the sudden onset of inflammatory pulmonary edema secondary to myriad local or systemic insults. The present article provides a review of current evidence in the epidemiology and treatment of acute lung injury and acute respiratory distress syndrome, with a focus on significant knowledge gaps that may be addressed through epidemiologic methods.Keywords: acute lung injury, acute respiratory distress syndrome, review, epidemiology

Published
2012

127. Does Monitoring Physician Work have Unintended Consequences?

Author

Summer, Ross and Summer, Ross

Abstract

Objectives: 1. Understand why physician work needs to be monitored. 2. Learn the most common method for measuring physician work. 3. Understand the potential unintended consequences that come from measuring physician work in academic medical centers. Presentation: 34 minutes

Published
2012

129. Cavin1; a Regulator of Lung Function and Macrophage Phenotype

Author

Govender, Praveen, primary, Romero, Freddy, additional, Shah, Dilip, additional, Paez, Jesus, additional, Ding, Shi-Ying, additional, Liu, Libin, additional, Gower, Adam, additional, Baez, Elizabeth, additional, Aly, Sherif Shawky, additional, Pilch, Paul, additional, and Summer, Ross, additional

Published
2013
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130. T-cadherin deficiency increases vascular vulnerability in T2DM through impaired NO bioactivity.

Author

Han Wang, Ling Tao, Ambrosio, Anastasia, Wenjun Yan, Summer, Ross, Bond Lau, Wayne, Yajing Wang, and Xinliang Ma

Subjects
CADHERINS, TYPE 2 diabetes, ENDOTHELIAL cells, VASCULAR endothelium, ATHEROSCLEROSIS
Abstract

Background: Endothelial dysfunction plays a critical role in the development of type 2 diabetes (T2DM). T-cadherin (T-cad) has gained recognition as a regulator of endothelial cell (EC) function. The present study examined whether T-cad deficiency increases vascular vulnerability in T2DM. Methods: Vascular segments were isolated from WT or T-cad knockout mice. Endothelial function, total NO accumulation, and the expression of T-cad related proteins were determined. Results: Ach and acidified NaNO2 induced similar vasorelaxation in WT groups. T-cad KO mice exhibited normal response to acidified NaNO2, but manifested markedly reduced response to Ach. NO accumulation was also decreased in T-cad KO group. T-cad expression was reduced in WT mice fed 8 weeks of high fat diet (HFD). Furthermore, exacerbated reduction of vasorelaxation was observed in T-cad KO mice fed 8 weeks of HFD. Conclusions: In the current study, we provide the first in vivo evidence that T-cadherin deficiency causes endothelial dysfunction in T2DM vascular segments, suggesting the involvement of T-cad deficiency in T2DM pathogenesis. [ABSTRACT FROM AUTHOR]

Published
2017
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135. Adiponectin Attenuates Lipopolysaccharide-Induced Acute Lung Injury through Suppression of Endothelial Cell Activation

Author

Konter, Jason M., primary, Parker, Jennifer L., additional, Baez, Elizabeth, additional, Li, Stephanie Z., additional, Ranscht, Barbara, additional, Denzel, Martin, additional, Little, Frederic F., additional, Nakamura, Kazuto, additional, Ouchi, Noriyuki, additional, Fine, Alan, additional, Walsh, Kenneth, additional, and Summer, Ross S., additional

Published
2012
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150. Acute respiratory distress syndrome: epidemiology and management approaches.

Author

Walkey, Allan J., Summer, Ross, Ho, Vu, and Alkana, Philip

Subjects
LUNG disease treatment, RESPIRATORY distress syndrome, PULMONARY edema, HYPOXEMIA, DISEASE incidence
Abstract

Acute lung injury and the more severe acute respiratory distress syndrome represent a spectrum of lung disease characterized by the sudden onset of inflammatory pulmonary edema secondary to myriad local or systemic insults. The present article provides a review of current evidence in the epidemiology and treatment of acute lung injury and acute respiratory distress syndrome, with a focus on significant knowledge gaps that may be addressed through epidemiologic methods. [ABSTRACT FROM AUTHOR]

Published
2012
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