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. Author manuscript; available in PMC: 2023 Jan 1.
Published in final edited form as: Gut. 2021 Jan 19:gutjnl-2020-323719. doi: 10.1136/gutjnl-2020-323719

Figure 6. Integrin β1 regulates pre-adipocyte migration on HIMC-derived extracellular matrix.

Figure 6.

(A) Blockade of integrin β1 significantly reduces migration of NL, UC, CDNS and CDS pre-adipocytes towards HIMC-conditioned medium in the Boyden chamber irrespective of the presence of TGF-β1. **P<0.01. (n=4–5)

(B) Left: Layout of wound healing assay of pre-adipocyte migration on HIMC-derived ECM. Right: Representative phase contrast images of wound closure by pre-adipocyte migration at baseline, 24h and 48h, and effect of GRGD, FAK inhibition and integrin β1 blockade on migration. (n=4–5).

(C) Wound closure was inhibited by GRGD, integrin β1 blocking antibody and FAK inhibitor for NL, UC, CDNS and CDS preadipocytes. (n=4–5).

(D) Representative tracking of pre-adipocytes seeded on HIMC-derived ECM was performed for 24h in the absence (control) and presence of GRGD, integrin β1 blocking antibody and FAK inhibitor. (n=4–5). A representative video can be found in the supplement (Video 2).

(E) Distance, displacement, velocity and migration persistence of pre-adipocyte migration on HIMC-derived ECM in untreated and following addition of GRGD, blocking antibodies to integrin β1 and FAK inhibitor. (n=4–5 with tracking n>50 cells per condition).

NL, Normal; UC, ulcerative colitis; CD, Crohn’s disease; CDNS: non-strictured Crohn’s disease; CDS: strictured Crohn’s disease. Focal adhesion kinase: FAK; statistically significant data are indicated by *P<0.05, **P<0.01, ***P<0.001,****P<0.0001.