C5a-Mediated Cell Migration In Vivo Protocol

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C5a-Mediated Cell Migration In Vivo Protocol

C5a plays a crucial role in the inflammatory response and immune regulation. Most of the biological functions of C5a depend on binding and activating the corresponding receptor C5aR. Studies have revealed that C5aR activation is closely linked to the remodeling of the cytoskeleton, which leads to increased cell motility and ligand-specific cell migration. Here, we describe a protocol for C5a-mediated cell migration in vitro.

Flow chart of C5a-mediated cell migration in vivo protocol. Fig.1 Flow chart of C5a-mediated cell migration in vivo protocol. (Creative Biolabs)

Published Data

C5a enhanced HSC chemotaxis. Fig.2 Complement C5a potentiates hematopoietic stem cell chemotaxis.1

Researchers investigated the contribution of complement C5a, a potent chemokine, to hepatic fibrosis by examining its effects on hepatic stellate cells (HSC), known to be pivotal in fibrogenesis. C5a was found not to modify HSC activation markers α-SMA and Col1A1. However, both wound healing and Boyden chamber assays revealed that C5a robustly enhanced HSC migration, exhibiting efficiency comparable to PDGF. Furthermore, C5a stimulated MCP-1 expression, and its induced migration was only partially impeded by an MCP-1 receptor antagonist, indicating the involvement of both MCP-1-dependent and independent pathways. These findings identify a novel complement-mediated mechanism driving HSC motility and suggest that targeting C5a signaling may offer therapeutic potential for liver fibrosis.

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Reference

  1. Das, Dola, Mark A. Barnes, and Laura E. Nagy. "Anaphylatoxin C5a modulates hepatic stellate cell migration." Fibrogenesis & Tissue Repair 7 (2014): 1-9. Distributed under Open Access license CC BY 2.0, without modification.
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