IndraLab

"This distribution change may allow outside-in signaling, because the integrin-beta1A+ D extracellular domains may allow interactions between (myo) fibroblasts and/or myocytes and the ECM to " sense " the mechanical wall stress of RV hypertension, septal shift, altered geometry, and increased fibrillar collagen, to trigger RV and septal HP biochemical signaling and ECM remodeling.26, 27 We previously identified the TGF-beta1 pathway as a central mediator of fibrosis in RV pressure load.13 TGF-beta1 binds integrin-beta1, which reciprocally activates latent TGF-beta1 and its profibrotic signaling.28, 29, 30 Consistent with our invitro results, integrin-beta1 inhibition in fibroblasts blocks TGF-beta1 activation and prevents fibrosis.31, 32 Activated TGF-beta1 induces collagen type I production through signaling cascades (eg, Smad2/3), which are active in our models.33, 34, 35, 36 This was supported by our invitro experiments that showed that blocking integrins decreased contractile activity of stretched fibroblasts."

"Interestingly, we also identified an interaction between TGFB1 from macrophages and ITGB1 from fibroblasts in HCM (Figure  xref )."

"Microglia not only received signals but also actively instructed other cell types, particularly oligodendrocytes, to enhance adhesion ( Tgfb1-Itgb1 , Lgals3bp-Itgb1 ) or lactate release ( Bsg-Slc16a1 ), possibly aiding in microglial metabolic reprogramming ( xref )."

"Remaining with CRT non-responders, we observed highly ranked CAF4 (enriched in CRT treated cases) and CAF5 interactions with antigen presenting cells (APCs) via IL33-IL1RL1, ANGPTL2-LILRB2 and TGFB1-ITGB1 was associated with changes in downstream target gene expression (Fig.  xref )."

"These results suggested that TNS4 may interact with ITGB1 on FRCs, thereby affecting the binding of TGF-β1 to ITGB1 and subsequently regulating the expression of a series of downstream signaling molecules (Fig.  xref E)."

"Top-ranked interactions included TGFB1-ITGB1 , VEGFA-FLT1 , and LAMA2-ITGA1 , suggesting si/p-cNMF2-high malignant cells may be engaged in the activation of perivascular and stromal niches ( xref - xref )."

"Our results indicated that TNS4 could interact with ITGB1 on FRCs, thereby affecting the binding of TGF-β1 to ITGB1 and subsequently regulating downstream signaling molecules, thus supporting the GC cell-induced LN metastasis (Fig.  xref H)."

"The most upregulated interactions all involve TGF-β1 signaling from AT2 cells, such as TGFB1-ITGB6, TNC-ITGAV, TGFB1-ITGB1 and TGFB1-TGFBR1/TGFBR2."

"Also, we identified a direct interaction between TGFB1 and ITGB1 and participated in laser irradiation-activated autophagy, thereby inhibiting UVB-mediated oxidative stress further reducing skin ageing."

"Notably, the interaction between ITGB1 and TGF-β1 can activate downstream signaling pathway molecules of TGF-β1, thus affecting a series of cellular biological processes, including the activation of fibroblasts [ xref ]."

"Spatial transcriptomic analyses revealed that si/p-cNMF1-high regions localized to high cell density, immune-rich tumor areas, whereas si/p-cNMF2-high regions occupied stromal and vascularized niches and co-occured with fibroblast and endothelial compartments enriched for TGFB1-ITGB1 , VEGFA-FLT1 , and LAMA2-ITGA1 signaling."

"Also, we identified a direct interaction between TGFB1 and ITGB1 and participated in laser irradiation-activated autophagy, thereby inhibiting UVB-mediated oxidative stress further reducing skin ageing."

"Furthermore, the axis TGFB2:TGFBR1/TGFBR2/TGFBR3 mediated interactions between cPCs and CD8 T cells together with TGFB1:ITGB1 (MAIT and NK with pPCs), suggesting a role of PCs in the immunosuppression of T-cell compartment."