Transforming growth factor-β2 (TGFβ2)-mediated epithelial to mesenchymal transition (EMT) in lens epithelial cells (LECs) has been implicated in fibrosis associated with secondary cataracts. In this study, we investigated whether the receptor for advanced glycation end products (RAGE) plays a role in TGFβ2-mediated EMT in LECs. Unlike in the LECs from wild-type mice, TGFβ2 failed to elicit an EMT response in LECs from RAGE knockout mice. The lack of RAGE also diminished TGFβ2-mediated Smad signaling. In addition, treatment with TGFβ2 increased IL-6 levels in LECs from wild-type mice but not in those from RAGE knockout mice. Treatment of human LECs with the RAGE inhibitor FPS-ZM1 reduced TGFβ2-mediated Smad signaling and the EMT response. Unlike that in wild-type lenses, the removal of fiber cell tissue in RAGE knockout lenses did not result in elevated levels of α-smooth muscle actin (α-SMA), fibronectin (FN), and integrin β1 in capsule-adherent LECs. Taken together, these results suggest that TGFβ2 signaling is intricately linked to RAGE. Targeting RAGE could be explored as a therapeutic strategy against secondary cataracts.
-
Cover Image
Cover Image
Autophagy is an important component of the innate immune response that restricts infection by different types of pathogens. In this issue Ylä-Anttila and Masucci (pp. 2297–2308) demonstrate the inhibition of selective autophagy by various members of the herpesvirus upiquitin-deconjugase family. The cover image shows representative micrographs illustrating the colocalization of SQSTM1/p62 (red) with LC3 (green) in cells expressing the viral enzymes (grey). The nuclei were stained with DAPI (blue). Size bars = 10 µm. Image provided by Maria G. Masucci.
Transforming growth factor-β2-mediated mesenchymal transition in lens epithelial cells is repressed in the absence of RAGE
Mi-Hyun Nam, Mina B. Pantcheva, Johanna Rankenberg, Ram H. Nagaraj; Transforming growth factor-β2-mediated mesenchymal transition in lens epithelial cells is repressed in the absence of RAGE. Biochem J 25 June 2021; 478 (12): 2285–2296. doi: https://doi.org/10.1042/BCJ20210069
Download citation file:
Sign in
Sign in to your personal account
Captcha Validation Error. Please try again.