C/EBP homologous protein–induced loss of intestinal epithelial stemness contributes to bile duct ligation–induced cholestatic liver injury in mice

Liu, Runping; Li, Xiaojiaoyang; Huang, Zhiming; Zhao, Derrick; Ganesh, Bhagyalaxmi Sukka; Lai, Guan–Hua; Pandak, William M.; Hylemon, Phillip B.; Bajaj, Jasmohan S.; Sanyal, Arun J.; Zhou, Huiping

doi:10.1002/hep.29540

Cited by 57 publications

(50 citation statements)

References 48 publications

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“…A previous study demonstrated that CHOP deficiency reduced bile duct ligation-induced disruption of tight junctions. This study reported no changes in mRNA and protein levels of tight junctions but did observe a mislocation of tight junction proteins such as occludin [297].…”

Section: Discussioncontrasting

confidence: 52%

The role of sphingosine kinase 2 in alcoholic liver disease

Kwong

Liu

Zhao

et al. 2019

Digestive and Liver Disease

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Alcoholic liver disease (ALD) is one of the most common liver diseases worldwide characterized by the accumulation of lipids within the liver, inflammation and the possibility of progressing to cirrhosis and liver failure. More importantly, there are currently no effective treatments for ALD and liver transplantation remains the only therapeutic option for end-stage liver disease. Previous studies have shown that ALD is a result of a combination of endoplasmic

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Section: Discussioncontrasting

confidence: 52%

The role of sphingosine kinase 2 in alcoholic liver disease

Kwong

Liu

Zhao

et al. 2019

Digestive and Liver Disease

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“…However, a recent study that used bile-duct ligation in mice as a model of cholestatic liver injury demonstrated that gut leakiness was associated with increased intestinal endoplasmic reticulum stress, intestinal epithelial cell apoptosis, and reduced expression of epithelial stem cell marker LGR5. 135 Nakamoto et al 127 demonstrated enrichment of Klebsiella pneumoniae in fecal samples from patients with PSC who also had ulcerative colitis. Colonization of mice with patient-derived fecal microbes showed that specific strains of K pneumoniae invaded the intestinal mucosa and increased gut leakiness, and were also found to induce pore formation in epithelial monolayer in vitro.…”

Section: Primary Sclerosing Cholangitismentioning

confidence: 99%

Contribution of the Intestinal Microbiome and Gut Barrier to Hepatic Disorders

2020

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Intestinal barrier dysfunction and dysbiosis contribute to development of diseases in liver and other organs. Physical, immunologic, and microbiologic (bacterial, fungal, archaeal, viral, and protozoal) features of the intestine separate its nearly 100 trillion microbes from the rest of the human body. Failure of any aspect of this barrier can result in translocation of microbes into the blood and sustained inflammatory response that promote liver injury, fibrosis, cirrhosis, and oncogenic transformation. Alterations in intestinal microbial populations or their functions can also affect health. We review the mechanisms that regulate intestinal permeability and how changes in the intestinal microbiome contribute to development of acute and chronic liver diseases. We discuss individual components of the intestinal barrier and how these are disrupted during development of different liver diseases. Learning more about these processes will increase our understanding of the interactions among the liver, intestine, and its flora.

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“…In contrast, the overexpression of transcription factor Chop exacerbated DSS-induced colitis, which seems due to impaired epithelial cell proliferation rather than increased apoptosis [ 27 ]. Consistently, a recent study showed that the absence of CHOP alleviates bile duct ligation-induced loss of stemness in intestinal stem cells, although the underlying mechanism is unclear [ 28 ]. Besides ER stress, eIF2 α phosphorylation serves as the regulatory hub of the so-called integrated stress response, which can also be initiated by three other serine/threonine eIF2 α kinases in response to distinct stimuli including viral infection (via the double-stranded RNA-activated protein kinase, a.k.a.…”

Section: Cellular Stress Signaling In Gastrointestinal Tractmentioning

confidence: 70%

Cellular Stress Responses and Gut Microbiota in Inflammatory Bowel Disease

Cao

2018

Gastroenterology Research and Practice

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Progresses in the past two decades have greatly expanded our understanding of inflammatory bowel disease (IBD), an incurable disease with multifaceted and challenging clinical manifestations. The pathogenesis of IBD involves multiple processes on the cellular level, which include the stress response signaling such as endoplasmic reticulum (ER) stress, oxidative stress, and hypoxia. Under physiological conditions, the stress responses play key roles in cell survival, mucosal barrier integrity, and immunomodulation. However, they can also cause energy depletion, trigger cell death and tissue injury, promote inflammatory response, and drive the progression of clinical disease. In recent years, gut microflora has emerged as an essential pathogenic factor and therapeutic target for IBD. Altered compositional and metabolic profiles of gut microbiota, termed dysbiosis, are associated with IBD. Recent studies, although limited, have shed light on how ER stress, oxidative stress, and hypoxic stress interact with gut microorganisms, a potential source of stress in the microenvironment of gastrointestinal tract. Our knowledge of cellular stress responses in intestinal homeostasis as well as their cross-talks with gut microbiome will further our understanding of the pathogenesis of inflammatory bowel disease and probably open avenues for new therapies.

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C/EBP homologous protein–induced loss of intestinal epithelial stemness contributes to bile duct ligation–induced cholestatic liver injury in mice

Cited by 57 publications

References 48 publications

The role of sphingosine kinase 2 in alcoholic liver disease

The role of sphingosine kinase 2 in alcoholic liver disease

Contribution of the Intestinal Microbiome and Gut Barrier to Hepatic Disorders

Cellular Stress Responses and Gut Microbiota in Inflammatory Bowel Disease

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