Fig 2: Effects of Rcn3-conditined media on adult cardiac fibroblasts (ACFs). (A) Experimental overview. (B) Expression of fibrosis-associated genes in ACFs and (C) Collagen I protein expressions in ACFs after treatment with control or Rcn3-conditioned media. (D) PI3K/Akt pathway activation in ACFs following treatment with Rcn3-conditioned media. Data represent mean ± SD from n = 3 independent biological replicates. n indicates independent experiments performed on separate days. TG, thapsigargin. * p < 0.05, ** p < 0.01, and *** p < 0.001.

Fig 3: Endoplasmic reticulum (ER) stress response in Jurkat cells. (A) Experimental overview. (B) Rcn3 gene and protein expression under ER stress. (C) Expression of ER stress-responsible genes in control and Rcn3-transducted Jurkat cells. Data represent mean ± SD from n = 3 independent biological replicates. n indicates independent experiments performed on separate days. TG, thapsigargin. ** p < 0.01, and *** p < 0.001.

Fig 4: Phenotype of T cell-specific Rcn3 conditional knockout (cKO) mice. (A) Experimental overview. (B) Rcn3 protein expression in the spleen. (C) Representative images of the transthoracic echocardiogram (TTE) at 1 and 21 days post-injury (dpi). (D) TTE analyses of cardiac function, including left ventricular ejection fraction (EF). Fibrosis-associated (E) gene and (F) protein expressions. (G) Histological analyses using Masson’s Trichrome staining. The scale bar in each figure represents 2000 μm. Infarct size was quantified from five sections per heart and averaged per mouse. n indicates individual mice. MI, myocardial infarction. * p < 0.05, ** p < 0.01, *** p < 0.001.