Expression dynamics of caveolin-1 in fibroblasts of newborn rats with chronic lung disease and its impact on lung fibroblast proliferation

Abstract

Purpose: To evaluate the changes of caveolin-1 in lung fibroblasts in newborn Wistar rats when exposed to hyperoxic conditions, as well as lung fibroblasts cell cycle. Methods: One hundred newborn Wistar rats were randomly divided (50 rats/group) into experimental and control groups, exposed to hyperoxic conditions or normal air, respectively. The fraction of inspired oxygen (FiO 2 ) in the experimental group was 90%, whereas this value was 21% in the control group. Lung fibroblasts were collected on days 3, 7, and 14 of the experiment. Caveolin-1 expression dynamics in lung fibroblasts was assayed in each group by immunofluorescence and Western blot analyses. Flow cytometry (FCM) was used to assess the proportions of lung fibroblasts at different stages of the cell cycle. Results: On day 3, no significant difference in caveolin-1 expression was observed between the hyperoxic and control groups; however, on days 7 and 14, caveolin-1 expression was significantly lower in the hyperoxic group than in the control (P<0.05). No apparent differences were observed in caveolin-1 expression in the control group at the different time points. Using FCM analysis, we showed that the proportion of lung fibroblasts in G0/G1 phase in the hyperoxic group decreased compared to that of the control group on day 7, while the proportion of S-phase cells increased (P<0.05). These differences were more significant when the groups were compared on day 14 (P<0.01). Conclusion: After seven days the exposure to hyperoxic conditions, lung fibroblasts proliferated and caveolin-1 expression decreased.

ERK1/2 Signaling Pathway Activated by EGF Promotes Proliferation, Transdifferentiation, and Migration of Cultured Primary Newborn Rat Lung Fibroblasts

“…LFs were used in experimental procedures when they became confluent, and showed a typical elongated and spindle-shaped appearance. LFs were identified by vimentin (sc-5565, 1 : 100; Santa Cruz Biotechnology, Santa Cruz, CA, USA) staining as we have published previously [ 13 ].…”

Certainties and uncertainties concerning the contribution of pericytes to the pathogenesis of systemic sclerosis

“…Although no clear evidence is yet available, pericytes lacking caveolin-1 may have impaired interactions with other vascular cells, including endothelial cells. Experiments involving murine models have shown a reduced expression of caveolin-1 in lung fibroblasts undergoing proliferation when exposed to hyperoxic conditions (52). Other authors have demonstrated that a deficit in caveolin-1 may induce mitochondrial dysfunction and accelerate the senescence of fibroblasts, thus leading in the generation of ROS and endothelial damage (53).…”