Evidence for modulation of pericryptal sheath myofibroblasts in rat descending colon by Transforming Growth Factor β and Angiotensin II.

Thiagarajah, Jay R.; Griffiths, N. M.; Pedley, Kevin C.; Naftalin, Richard J

doi:10.1186/1471-230x-2-4

Cited by 12 publications

(12 citation statements)

References 57 publications

(65 reference statements)

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“…NAD(P)H oxidase 4 mediates TGFβ transdifferentiation in cardiac fibroblasts (44), as does the urokinase plasminogen activator/urokinase plasminogen activator receptor system in corneal stromal cells (45) and NK2 in lung fibroblasts (see above). α-SMA is upregulated in intestinal pericryptal myofibroblasts by low-salt diet and by nonlethal radiation exposure, a phenomenon that is blocked by captopril, an angiotensin-converting enzyme inhibitor (46). Prostaglandin E 2 (PGE 2 ) inhibits fibroblast-myofibroblast transition through prostanoid EP2 receptors coupled to cyclic AMP (cAMP) production (47).…”

Section: Origin Of Myofibroblasts and Mural Cellsmentioning

confidence: 99%

Mesenchymal Cells of the Intestinal Lamina Propria

Powell

Pinchuk

Saada

et al. 2011

Annu. Rev. Physiol.

337

358

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The mesenchymal elements of the intestinal lamina propria reviewed here are the myofibroblasts, fibroblasts, mural cells (pericytes) of the vasculature, bone marrow–derived stromal stem cells, smooth muscle of the muscularis mucosae, and smooth muscle surrounding the lymphatic lacteals. These cells share similar marker molecules, origins, and coordinated biological functions previously ascribed solely to subepithelial myofibroblasts. We review the functional anatomy of intestinal mesenchymal cells and describe what is known about their origin in the embryo and their replacement in adults. As part of their putative role in intestinal mucosal morphogenesis, we consider the intestinal stem cell niche. Lastly, we review emerging information about myofibroblasts as nonprofessional immune cells that may be important as an alarm system for the gut and as a participant in peripheral immune tolerance.

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Section: Origin Of Myofibroblasts and Mural Cellsmentioning

confidence: 99%

Mesenchymal Cells of the Intestinal Lamina Propria

Powell

Pinchuk

Saada

et al. 2011

Annu. Rev. Physiol.

337

358

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“…Low-Na adaptation increased the expression of ␣-smooth muscle actin, specific adhesion molecules such as OB-cadherin, and collagen IV in the pericryptal sheath (4,17,33), and also resulted in functional changes in the crypt epithelium, including increased expression of junctional proteins such as claudin IV and E-cadherin. These effects were mediated by the mineralocorticoid receptor (MR) because spironolactone (SPI) prevented the effects of Aldo (4,17).…”

mentioning

confidence: 99%

Aldosterone induces myofibroblast EGF secretion to regulate epithelial colonic permeability

Miró

Pérez-Bosque

Maijó

et al. 2013

American Journal of Physiology-Cell Physiology

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Miró L, Pérez-Bosque A, Maijó M, Amat C, Naftalin RJ, Moretó M. Aldosterone induces myofibroblast EGF secretion to regulate epithelial colonic permeability. Am J Physiol Cell Physiol 304: C918-C926, 2013. First published March 6, 2013; doi:10.1152 doi:10. /ajpcell.00292.2012 show that raised aldosterone (Aldo) during low-Na adaptation regulates the growth of pericryptal myofibroblasts and reduces the permeability of the colonic epithelium. The aim of this study was to reproduce in vitro the in vivo condition of increased Aldo using human CCD-18Co myofibroblasts and T84 colonic epithelial cells to measure myofibroblast and epithelial proliferation and the expression of intercellular junction proteins. Proliferation was quantified by measuring 5-bromo-2=-deoxyuridine incorporation. The myofibroblast expression of EGF, VEGFa, and transforming growth factor-␤1 (TGF-␤1) was measured by real-time PCR and the expression of junctional complex proteins by Western blot. Aldo stimulated the proliferation of myofibroblasts by 70% (P Ͻ 0.05) and increased EGF mRNA expression by 30% (P Ͻ 0.05) without affecting VEGFa and TGF-␤1. EGF concentration in the incubation medium increased by 30% (P Ͻ 0.05) 24 h after Aldo addition, and these effects were prevented by the addition of spironolactone. Myofibroblast proliferation in response to Aldo was mediated by EGF receptor (EGFR) and involved both MAPKK and phosphatidylinositol 3-kinase pathways. When T84 cells were incubated with medium from myofibroblasts stimulated with Aldo (conditioned medium), the expression of ␤-catenin and claudin IV was increased by 30% (P Ͻ 0.05) and proliferation by 40% (P Ͻ 0.05). T84 proliferation decreased when ␣-EGF, or the EGFR antagonist AG1478, was present. Results in vivo indicate that rats fed a low-salt diet showed an increased expression of EGF and EGFR in the colonic mucosa. These results support the view that changes in colonic permeability during low-Na adaptation are mediated by the EGF secreted by myofibroblasts in response to raised Aldo. aldosterone; EGF; proliferation THE CRYPTS IN THE DESCENDING colon can absorb fluid despite a high hydraulic resistance in the lumen. The capacity to absorb a hypertonic absorbate requires Na pump activity and a physical barrier to Na movement from the pericryptal space into the submucosa and pericryptal capillaries to maintain a high osmotic pressure gradient across the crypt mucosa (19). This physical barrier is called the pericryptal sheath and is made up of a network of myofibroblast-like cells and the extracellular matrix surrounding the colonic crypts (13,19,22).Low-Na intake activates the renin-angiotensin-aldosterone system (RAAS), which increases both angiotensin II (ANG II) and aldosterone (Aldo) plasma concentration. Activation of the RAAS increases colonic fluid and Na absorption (31). These effects are partly due to the upregulation of the epithelial sodium channel (ENaC) and changes in the barrier function of the pericryptal sheath, as has been shown in both rat and mouse descending colonic...

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“…When Na + intake diminishes, the renin–angiotensin–aldosterone system is activated, and this results in increased colonic Na + absorption, decreased epithelial permeability and stimulation of pericryptal myofibroblast growth (Thiagarajah et al . ). Myofibroblast proliferation is regulated by many growth factors and cytokines (Powell et al .…”

Section: Introductionmentioning

confidence: 97%

“…; Thiagarajah et al . ) as well as systemic hormones, such as aldosterone (Cristià et al . ; Moretó et al .…”

Section: Introductionmentioning

confidence: 99%

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Vasopressin regulation of epithelial colonic proliferation and permeability is mediated by pericryptal platelet‐derived growth factor A

Miró

Pérez-Bosque

Maijó

et al. 2014

Experimental Physiology

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New Findings r What is the central question of this study?Arginine vasopressin (AVP) regulates distal colonic crypt cell proliferation and permeability in vivo, but the underlying mechanism is poorly understood. Our study addresses whether AVP is acting directly on myofibroblasts and enterocytes or by mechanisms involving local regulators, in an in vitro model using human myofibroblasts and enterocyte cell lines. r What is the main finding and its importance?The effect of AVP in stimulating myofibroblast proliferation involves pericryptal platelet-derived growth factor A, which mediates local effects by an autocrine loop and epithelial proliferation and permeability by a paracrine mechanism. These data highlight the role of growth factors as local mediators of systemic hormones.Arginine vasopressin (AVP) has trophic effects on the rat distal colon, increasing the growth of pericryptal myofibroblasts and reducing the colonic crypt wall permeability. This study aimed to reproduce in vitro the effects of AVP observed in vivo using cultures of human CCD-18Co myofibroblasts and T84 colonic epithelial cells. Proliferation of myofibroblasts was quantified by bromodeoxyuridine incorporation; the expression of platelet-derived growth factor A (PDGFA), platelet-derived growth factor B, epidermal growth factor, transforming growth factor-β and vascular endothelial growth factor was measured by PCR and the expression of epithelial junction proteins by Western blot. Arginine vasopressin stimulated myofibroblast proliferation and the expression of PDGFA without affecting the expression of platelet-derived growth factor B, epidermal growth factor, transforming growth factor-β or vascular endothelial growth factor. These effects were prevented when AVP receptor inhibitors were present in the medium. Pre-incubation of CCD-18Co cells with anti-PDGF antibody or with an inhibitor of the PDGF receptor abolished the effects of AVP. When colonocytes were incubated with medium obtained from myofibroblasts incubated with AVP, both cell proliferation and the expression of epithelial junction proteins increased; however, direct incubation of colonocytes with AVP did not modify these variables. These results demonstrate that AVP stimulates myofibroblast proliferation and induces PDGFA secretion, implying that PDGFA mediates local myofibroblast proliferation by L. Miró and A. Pérez-Bosque contributed equally to this work.

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Evidence for modulation of pericryptal sheath myofibroblasts in rat descending colon by Transforming Growth Factor β and Angiotensin II.

Cited by 12 publications

References 57 publications

Mesenchymal Cells of the Intestinal Lamina Propria

Mesenchymal Cells of the Intestinal Lamina Propria

Aldosterone induces myofibroblast EGF secretion to regulate epithelial colonic permeability

Vasopressin regulation of epithelial colonic proliferation and permeability is mediated by pericryptal platelet‐derived growth factor A

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