Posthemorrhagic shock mesenteric lymph enhances monolayer permeability via F-actin and VE-cadherin

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• 作者：Gai-Xia Sun ; MMS¹ ; Ya-Xiong Guo ; PhD¹ ; Yu-Ping Zhang ; MMS ; Li-Min Zhang ; MMS ; Zi-Gang Zhao ; PhD ; Chun-Yu Niu ; PhD ; ^{ncylxf@126.com" class="auth_mail" title="E-mail the corresponding author}
• 关键词：Hemorrhagic shock ; Lymph ; Permeability ; Human umbilical vein endothelial cells ; F-actin ; VE-cadherin
• 刊名：Journal of Surgical Research
• 出版年：2016
• 出版时间：1 June 2016
• 年：2016
• 卷：203
• 期：1
• 页码：47-55
• 全文大小：2317 K

文摘

Vascular hyperpermeability plays a critical role in the development of refractory hypotension after severe hemorrhagic shock. Posthemorrhagic shock mesenteric lymph (PHSML) return has been shown to be involved in regulation of vascular hyperpermeability. The present study was conducted to investigate the effect of PHSML on permeability of endothelial cells in vitro.

Materials and methods

A hemorrhagic shock model (40 ± 2 mm Hg for 90 min, followed by fluid resuscitation) was used for collection of PHSML. Two separated PHSMLs were collected from period 0–3 h (early) and period 3–6 h (late) after resuscitation and diluted into concentration of 4% or 10%. The human umbilical vein endothelial cells (HUVECs) were then treated with these PHSMLs for 6 h. The monolayer cellular permeability to FITC-albumin was observed by using the costar transwell system. The multiple approaches including scanning electron microscope, fluorescent cytochemistry staining, and Western blotting were also used to assess the changes in cellular morphologic and the expressions of F-actin and VE-cadherin.

Results

The treatments with either early or late PHSML resulted in morphologic injuries, increased cellular permeability, and decreased expression of F-actin in HUVECs. In contrast, only early PHSML, but not late PHSML, reduced the VE-cadherin expression.

Conclusions

These results indicate that the PHSML in vitro increases the cellular permeability of HUVECs through suppression of F-actin and VE-cadherin.