Fig. 2

Lactate promoted proliferation and migration of mPASMCs in an LDHA-dependent manner under hypoxia. (A) The effect on mPASMCs viability was assessed using the CCK-8 assay after treatment with lactate for 0, 24 and 48 h at various concentrations (0, 5, 10, and 20 mM). (B) The impact of lactate-induced mPASMC proliferation at different concentrations (0, 5, 10, and 20 mM) was evaluated following 24 h of lactate treatment using the EdU incorporation assay. Representative images (B1) and quantification (B2) of the EdU assay in mPASMCs were presented. (C) Representative images of Western blots and the combined quantitative data (below) show the expression of PCNA and Cyclin D1 in mPASMCs after treatment with lactate for 24 h at different concentrations (0, 5, 10, and 20 mM). (D) Representative images (D1) of the wound healing assay of mPASMCs in vitro and quantification (D2) of the wound healing assay of mPASMCs after treatment with lactate for 0, 24 and 48 h at different concentrations (0, 5, 10, and 20 mM). (E) Lactate levels in the cell supernatants of mPASMCs were measured for each group. (F) The viability of mPASMCs in each group was evaluated using the CCK-8 assay. (G) The impact of LDHA on mPASMCs proliferation under normoxia or hypoxia was evaluated using the EdU incorporation assay, as depicted in representative images (G1) and quantification (G2) of the EdU assay of mPASMCs. (H) The Effect of LDHA on mPASMCs migration was measured by wound healing assay under normoxia or hypoxia, shown in representative images (H1) and quantification data (H2). Data were presented as Mean ± SD. n = 4–6, NS: no statistical signification, **p < 0.01