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Heat stress combined with lipopolysaccharide induces pulmonary microvascular endothelial cell glycocalyx inflammatory damage in vitro
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  • Jiadi Chen,
  • Ding Chengjia,
  • Cao Jingjing,
  • Chen Yi,
  • Tong Huasheng
Jiadi Chen
The First Affiliated Hospital of Shantou University Medical College
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Ding Chengjia
Binhaiwan Central Hospital of Dongguan
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Cao Jingjing
Binhaiwan Central Hospital of Dongguan
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Chen Yi
Binhaiwan Central Hospital of Dongguan

Corresponding Author:[email protected]

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Tong Huasheng
PLA General Hospital of Southern Theatre Command
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Abstract

Heat stroke is a life-threatening disease with high mortality rate and unexpected complications. Vascular endothelial glycocalyx is essential for maintaining endothelial cell structure and function as well as preventing adhesion of inflammatory cells. Potential relationship that underlays the imbalance in inflammation and coagulation remains elusive. Moreover, the role of endothelial glycocalyx in heat stroke-induced organ injury remained unclear. Heat stress and lipopolysaccharide (LPS) are employed to construct in vitro models to study the change of glycocalyx structure and function in human pulmonary microvascular endothelial cells (HPMEC), as well as levels of heparansulfate proteoglycan (HSPG), syndecans-1, heparansulfate, TNF-α, IL-6, vWF, ET-1, Occludin, E-selectin, vascular cell adhesion molecule-1 (VCAM-1), and reactive oxygen species (ROS). Here, we showed that heat stress and LPS devastated endothelial glycocalyx structure, activated endothelial glycocalyx degradation, and triggered oxidative damage in addition to apoptosis in HPMEC. Stimulation of heat stress and LPS increased HSPG, syndecans-1 (SDC-1), and heparansulfate levels, and promoted the ability to produce and release pro-inflammation cytokines (TNF-α, IL-6,) and coagulative factor (vWF, ET-1) in HPMEC. Furthermore, E-selectin, VCAM-1, and ROS expression were upregulated in contrast to Occludin downregulation. These changes could be deteriorated by Heparanase, whereas could be ameliorated by unfractionated heparin. This study highlights that heat stroke-induced endothelial glycocalyx degradation can trigger oxidative and apoptosis in HPMEC, in addition to dysfunction of inhibition of inflammatory response and protection in vascular permeability.
03 Jan 2023Submitted to Immunity, Inflammation and Disease
06 Jan 2023Submission Checks Completed
06 Jan 2023Assigned to Editor
06 Jan 2023Review(s) Completed, Editorial Evaluation Pending
10 Jan 2023Reviewer(s) Assigned
24 Feb 2023Editorial Decision: Revise Major
26 Apr 20231st Revision Received
27 Apr 2023Submission Checks Completed
27 Apr 2023Assigned to Editor
27 Apr 2023Review(s) Completed, Editorial Evaluation Pending
01 May 2023Reviewer(s) Assigned
29 May 2023Editorial Decision: Revise Major
29 Jun 20232nd Revision Received
30 Jun 2023Assigned to Editor
30 Jun 2023Submission Checks Completed
30 Jun 2023Review(s) Completed, Editorial Evaluation Pending
06 Jul 2023Reviewer(s) Assigned
15 Sep 2023Editorial Decision: Accept