scholarly journals c-MAF maintains the transcriptional program of enterocyte zonation and the balance of absorptive/intestinal secretory cell types

2021 ◽  
Author(s):  
Alejandra González-Loyola ◽  
Tania Wyss ◽  
Olivia Munoz ◽  
Borja Prat-Luri ◽  
Mauro Delorenzi ◽  
...  
Keyword(s):  
Body Weight ◽  
Molecular Mechanisms ◽  
Body Weight Loss ◽  
Cell Types ◽  
Intestinal Injury ◽  
Lipid Absorption ◽  
Bile Acid Metabolism ◽  
Tuft Cell ◽  
Small Intestinal ◽  
Factor C

AbstractSmall intestinal villi are structural and functional units uniquely adapted to the nutrient absorption in higher vertebrates. Villus enterocytes are organized in spatially resolved “zones” dedicated to specialized tasks such anti-bacterial protection, and absorption of amino-acids, carbohydrates and lipids. The molecular mechanisms specifying villus zonation are incompletely understood. We report that inactivation of transcription factor c-MAF, highly expressed in mature lower and mid-villus enterocytes, perturbed the entire villus zonation program, by increasing the expression of regulators of carbohydrate and bile acid metabolism and transport, while suppressing genes related to amino acid and lipid absorption. Maf inactivation under homeostatic conditions expanded tuft cells and led to compensatory gut lengthening, preventing body weight loss. However, delayed enterocyte maturation in the absence of Maf impaired body weight recovery after acute intestinal injury, resulting in reduced survival. Our results identify c-MAF as a novel regulator of small intestinal villus zonation program, while highlighting the importance of coordination between stem/progenitor and differentiation programs for intestinal regeneration.Summaryc-MAF is expressed in differentiated enterocytes. c-MAF loss alters enterocyte zonation leading to a compensatory gut remodelling and tuft cell expansion. Upon acute intestinal injury mice deficient for c-MAF cannot recover due to lack of nutrient transport and compensatory lengthening.

scholarly journals Tanshinone IIA Sodium Sulfonate Attenuates LPS-Induced Intestinal Injury in Mice

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Xin-Jing Yang ◽  
Jin-Xian Qian ◽  
Yao Wei ◽  
Qiang Guo ◽  
Jun Jin ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Intestinal Injury ◽  
Beclin 1 ◽  
Tanshinone Iia ◽  
Inflammatory Factors ◽  
Rt Pcr ◽  
Intestinal Tissue ◽  
Sodium Sulfonate ◽  
Small Intestinal Injury ◽  
Small Intestinal

Background. Tanshinone IIA sodium sulfonate (TSS) is known to possess anti-inflammatory effects and has exhibited protective effects in various inflammatory conditions; however, its role in lipopolysaccharide- (LPS-) induced intestinal injury is still unknown. Objective. The present study is designed to explore the role and possible mechanism of TSS in LPS-induced intestinal injury. Methods. Male C57BL/6J mice, challenged with intraperitoneal LPS injection, were treated with or without TSS 0.5 h prior to LPS exposure. At 1, 6, and 12 h after LPS injection, mice were sacrificed, and the small intestine was excised. The intestinal tissue injury was analyzed by HE staining. Inflammatory factors (TNF-α, IL-1β, and IL-6) in the intestinal tissue were examined by ELISA and RT-PCR. In addition, expressions of autophagy markers (microtubule-associated light chain 3 (LC3) and Beclin-1) were detected by western blot and RT-PCR. A number of autophagosomes were also observed under electron microscopy. Results. TSS treatment significantly attenuated small intestinal epithelium injury induced by LPS. LPS-induced release of inflammatory mediators, including TNF-α, IL-1β, and IL-6, were markedly inhibited by TSS. Furthermore, TSS treatment could effectively upregulate LPS-induced decrease of autophagy levels, as evidenced by the increased expression of LC3 and Beclin-1, and more autophagosomes. Conclusion. The protective effect of TSS on LPS-induced small intestinal injury may be attributed to the inhibition of inflammatory factors and promotion of autophagy levels. The present study may provide novel insight into the molecular mechanisms of TSS on the treatment of intestinal injury.

scholarly journals EFFECT OF AMLODIPINE ON ENTEROPATHY INDUCED BY INDOMETHACIN IN RATS

2020 ◽  
pp. 144-150
Author(s):  
YARA ANNOUF ◽  
SHAZA AL-LAHAM ◽  
EYAD AL-SHATTI
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Small Intestine ◽  
Body Weight Loss ◽  
Antioxidant Defenses ◽  
Length Ratio ◽  
Intestinal Damage ◽  
Sod Activity ◽  
Small Intestinal Injury ◽  
Small Intestinal

Objective: Non-steroidal anti-inflammatory drugs (NSAIDs) have become well known for causing gastroduodenal mucosal damage. In addition, they are also known to affect the small intestine in humans. Amlodipine is a third-generation dihydropyridine-type calcium channel blocker; it can inhibit inflammatory cytokines and enhance antioxidant defenses. The aim of this study was to evaluate the effect of Amlodipine on indomethacin-induced enteropathy in rats. Methods: Enteropathy was induced by subcutaneous indomethacin (Indo) prepared in 5 % sodium bicarbonate administrated at a dose rate of 9 mg/kg for two days at 24h intervals. Amlodipine (10 mg/Kg body weight po) was administrated for seven consecutive days beginning 24 h after the first Indo injection. Rats were sacrificed under ether anesthesia on the 8th day. The small intestinal injury was assessed by body weight loss, small intestine weight/length ratio, macroscopic damage, histological study, as well as by biochemical measurement of reduced glutathione (GSH), lipid peroxides and superoxide dismutase (SOD) activity in the small intestine tissue. Results: The results showed that Amlodipine didn't decrease body weight loss, it decreased small intestine weight/length ratio, macroscopic and microscopic small intestinal damage scores caused by administration of Indo. It also increased SOD activity and decreased lipid peroxidation. The effect on the level of GSH wasn't observed. No statistical significance was observed when previous findings were compared to Indo induced enteropathy group (p>0.05). Conclusion: Amlodipine didn't produce an obvious enhancement in enteropathy induced by Indo in rats.

1965-P: Glucagon Receptor Agonism Stimulates Body Weight Loss in Antibiotic Treatment in Obese Mice

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1965-P
Author(s):  
TEAYOUN KIM ◽  
JESSICA P. ANTIPENKO ◽  
SHELLY NASON ◽  
NATALIE PRESEDO ◽  
WILLIAM J. VAN DER POL ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Antibiotic Treatment ◽  
Body Weight Loss ◽  
Obese Mice ◽  
Glucagon Receptor

Relation between change in treatment for central diabetes insipidus and body weight loss

2018 ◽  
Vol 44 (1) ◽  
Author(s):  
Ayako Ito ◽  
Aya Nozaki ◽  
Ichiro Horie ◽  
Takao Ando ◽  
Atsushi Kawakami
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Diabetes Insipidus ◽  
Body Weight Loss ◽  
Central Diabetes Insipidus

scholarly journals Anaphylactic Degranulation of Mast Cells: Focus on Compound Exocytosis

2019 ◽  
Vol 2019 ◽  
pp. 1-12 ◽  
Author(s):  
Ofir Klein ◽  
Ronit Sagi-Eisenberg
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Molecular Mechanisms ◽  
Secretory Granules ◽  
Cell Types ◽  
Secretory Cells ◽  
Regulated Exocytosis ◽  
Open Questions ◽  
Conflicting Evidence ◽  
Compound Exocytosis

Anaphylaxis is a notorious type 2 immune response which may result in a systemic response and lead to death. A precondition for the unfolding of the anaphylactic shock is the secretion of inflammatory mediators from mast cells in response to an allergen, mostly through activation of the cells via the IgE-dependent pathway. While mast cells are specialized secretory cells that can secrete through a variety of exocytic modes, the most predominant mode exerted by the mast cell during anaphylaxis is compound exocytosis—a specialized form of regulated exocytosis where secretory granules fuse to one another. Here, we review the modes of regulated exocytosis in the mast cell and focus on compound exocytosis. We review historical landmarks in the research of compound exocytosis in mast cells and the methods available for investigating compound exocytosis. We also review the molecular mechanisms reported to underlie compound exocytosis in mast cells and expand further with reviewing key findings from other cell types. Finally, we discuss the possible reasons for the mast cell to utilize compound exocytosis during anaphylaxis, the conflicting evidence in different mast cell models, and the open questions in the field which remain to be answered.

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