Journal
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
Volume 24, Issue 11, Pages -Publisher
MDPI
DOI: 10.3390/ijms24119110
Keywords
blacktip shark collagen; mesenchymal stem cells; integrin; marine biomaterials; extracellular matrix
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Marine collagen has been gaining attention as a biomaterial substitute in tissue engineering due to its role in cellular signaling mechanisms, especially in mesenchymal stem cells (MSCs). This study investigated the integrin receptor binding mechanism and proliferation of MSCs when exposed to marine collagen derived from blacktip reef shark and blue shark compared to bovine collagen. The results showed that marine collagen enhanced MSC proliferation, adhesion, and shape maintenance by interacting with specific integrin subunits, triggering further signaling cascade mechanisms.
Marine collagen (MC) has recently attracted more attention in tissue engineering as a biomaterial substitute due to its significant role in cellular signaling mechanisms, especially in mesenchymal stem cells (MSCs). However, the actual signaling mechanism of MC in MSC growth, which is highly influenced by their molecular pattern, is poorly understood. Hence, we investigated the integrin receptors (alpha(1)beta(1), alpha(2)beta(1), alpha(10)beta(1), and alpha(11)beta(1)) binding mechanism and proliferation of MCs (blacktip reef shark collagen (BSC) and blue shark collagen (SC)) compared to bovine collagen (BC) on MSCs behavior through functionalized collagen molecule probing for the first time. The results showed that BSC and SC had higher proliferation rates and accelerated scratch wound healing by increasing migratory rates of MSCs. Cell adhesion and spreading results demonstrated that MC had a better capacity to anchor MSCs and maintain cell morphology than controls. Living cell observations showed that BSC was gradually assembled by cells into the ECM network within 24 h. Interestingly, qRT-PCR and ELISA revealed that the proliferative effect of MC was triggered by interacting with specific integrin receptors such as alpha(2)beta(1), alpha(10)beta(1), and alpha(11)beta(1) of MSCs. Accordingly, BSC accelerated MSCs' growth, adhesion, shape, and spreading by interacting with specific integrin subunits (alpha(2) and beta(1)) and thereby triggering further signaling cascade mechanisms.
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