Mesothelial cells and peritoneal homeostasis

Mutsaers, Steven E.; Prêle, Cecilia M.; Pengelly, Steven; Herrick, Sarah E.

doi:10.1016/j.fertnstert.2016.09.005

Cited by 111 publications

(94 citation statements)

References 74 publications

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“…Intestinal adhesion is a common complication of abdominal surgery. Patients would have no symptoms if adhesion presents as “static.” However, patients can suffer from serious consequences, such as intestinal obstruction, female infertility, chronic abdominal pain, bowel necrosis, and even death (Charboneau et al, ; Mutsaers, Prele, Pengelly, & Herrick, ; Sisodia et al, ). Several strategies have been used to prevent postoperative intestinal adhesion, especially antiadhesive materials, such as SH (Di Saverio et al, ; Mahdy, Mohamed, & Elhawary, ; Montalvo‐Jave et al, ; Panahi et al, ; Vrijland, Tseng, Eijkman, et al, ).…”

Section: Discussionmentioning

confidence: 99%

Platelet‐rich fibrin prevents postoperative intestinal adhesion

Jia

Guo

et al. 2020

J Biomedical Materials Res

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Platelet‐rich fibrin (PRF) was prepared from the blood of BALB/C inbred mice to explore potential effects on postoperative intestinal adhesion. A murine model of intestinal adhesion characterized by abdominal wall defect/and cecum damage was established by scraping caecum serosa and cutting peritoneum and muscles in the abdominal wall. The wound was covered with PRF (group A), sodium hyaluronate (group B), or left alone (blank control; group C). All animals were monitored for 28 days. The incidence of adhesion was 35.0, 66.7, and 73.7% in groups A, B, and C, respectively. The incidence of adhesion in group A was significantly lower than that in group C (p < .05). Histopathologically, severity of fibrosis and the number of fibroblasts or inflammatory cells in group A were lower than those in groups B and C (p < .05), whereas the number of mesothelial cells was higher (p = .001). Furthermore, the severity of fibrosis and number of fibroblasts or inflammatory cells were lower in low grade than those in high grade of adhesion (p < .05), whereas the number of mesothelial cells was higher (p < .05). Collectively, PRF applied to abdominal surgery may reduce the incidence of intestinal adhesion by promoting proliferation of mesothelial cells whereas inhibiting proliferation of fibroblasts and infiltration of inflammatory cells.

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Section: Discussionmentioning

confidence: 99%

Platelet‐rich fibrin prevents postoperative intestinal adhesion

Jia

Guo

et al. 2020

J Biomedical Materials Res

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“…The success of PD is largely dependent on the structural and functional integrity of mesothelium, which is formed by a monolayer of PMCs [26]. However, an important problem associated with PD is a time-dependent limitation of peritoneal function including loss of peritoneal membrane integrity and peritoneal ultrafiltration capacity [27].…”

Section: Discussionmentioning

confidence: 99%

Sulfotanshinone IIA Sodium Ameliorates Glucose Peritoneal Dialysis Solution-Induced Human Peritoneal Mesothelial Cell Injury via Suppression of ASK1-P38-mediated Oxidative Stress

Zhou

Sun

et al. 2018

Cell Physiol Biochem

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Background/Aims: Long-term use of high-glucose peritoneal dialysis solution (PDS) induces peritoneal mesothelial cell (PMC) injury, peritoneal dysfunction, and peritoneal dialysis (PD) failure in patients with end-stage renal disease. How to preserve PMCs in PD is a major challenge for nephrologists worldwide. In this study, we aimed to elucidate the efficacy and mechanisms of sulfotanshinone IIA sodium (Tan IIa) in ameliorating high-glucose PDS-induced human PMC injury. Methods: The human PMC line HMrSV5 was incubated with 4.25% PDS in vitro to mimic the high-glucose conditions in PD. Cellular viability was measured by Cell Counting Kit 8. Generation of superoxide and reactive oxygen species (ROS) was assessed using a Total ROS/Superoxide Detection Kit. Oxidative modification of protein was evaluated by OxyBlot Protein Oxidation Detection Kit. TUNEL (dT-mediated dUTP nick end labeling) assay and DAPI (4,6-diamidino-2-phenylindole) staining were used to evaluate apoptosis. Western blot analysis was performed to evaluate the efficacy and mechanisms of Tan IIa. Results: Tan IIa protected PMCs against PDS-induced injury as evidenced by alleviating changes in morphology and loss of cell viability. Consistent with their antioxidant properties, N-acetyl-L-cysteine (NAC) and Tan IIa suppressed superoxide and ROS production, protein oxidation, and apoptosis elicited by PDS. Apoptosis signal-regulating kinase 1 (ASK1)-p38 signaling was activated by PDS. Both Tan IIa and NAC suppressed ASK1 and p38 phosphorylation elicited by PDS. Moreover, genetic downregulation of ASK1 ameliorated cell injury and inhibited the phosphorylation of p38 and activation of caspase 3. Conclusion: Tan IIa protects PMCs against PDS-induced oxidative injury through suppression of ASK1-p38 signaling.

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“…Mesothelial healing progresses diffusely across the exposed surface, whereas for other epithelia, healing occurs by centripetal migration of cells from the wound edge. A free-floating population of mesothelial cells migrates and attaches to injured serosa [24] [25]. The perivascular location of dermal mesothelial cells may reflect their pathway of arrival and/or signify their importance in granulation tissue angiogenesis and vascular remodeling.…”

Section: Discussionmentioning

confidence: 99%

Investigation of Open Abdomen Visceral Skin Graft Revascularization and Separation from Peritoneal Contents

Clark¹,

Coffman²,

Brandenburg³

et al. 2018

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Background: Despite increasing survival following damage control laparotomy and open abdomen technique, little is known about the biology of visceral skin graft revascularization and separation from peritoneal contents. Methods: Following laparotomy for trauma, patients with visceral edema preventing fascial closure underwent Vicryl mesh closure followed by visceral split-thickness skin grafting and readmission graft excision and abdominal wall reconstruction. Utilizing laser speckle contrast imaging, immunochemical staining of histologic sections, and RT-PCR array technology, we examined the revascularization, microvascular anatomy, morphology, and change in gene expression of visceral skin grafts. Results: Ten patients ranging in age from 25 to 46 years underwent visceral grafting for cutaneous coverage of an open abdomen. Skin graft perfusion peaked at a mean of 350 PU by post-operative day 14 synchronous with closure of meshed interstices, and remained constant until excision. Time to graft excision ranged from 6 to 18 months. CD-31 immunostaining documented a significant (p = 0.04) increase in vascular surface area in excised grafts compared to control skin. Trichrome staining revealed an 8-fold increase in excised graft thickness. Mesothelial cells were identified within the dermal matrix of excised grafts. RT-PCR demonstrated significant up-regulation of genes involved in matrix structure and remodeling, cytoskeleton regulation, and WNT signaling; and down-regulation of genes involved in inflammation and matrix proteolysis in excised grafts compared to control skin. Conclusion: Our data document early visceral skin graft perfusion and a plateau in revascularization. Histology reveals a robust dermal matrix populated by fibroblasts and mesothelial cells within a complex supporting vascular network. Genetic analysis of excised grafts reveals growth factor, collagen, and matrix remodeling gene expression.

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Mesothelial cells and peritoneal homeostasis

Cited by 111 publications

References 74 publications

Platelet‐rich fibrin prevents postoperative intestinal adhesion

Platelet‐rich fibrin prevents postoperative intestinal adhesion

Sulfotanshinone IIA Sodium Ameliorates Glucose Peritoneal Dialysis Solution-Induced Human Peritoneal Mesothelial Cell Injury via Suppression of ASK1-P38-mediated Oxidative Stress

Investigation of Open Abdomen Visceral Skin Graft Revascularization and Separation from Peritoneal Contents

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