Fig. 6: PICALM functioned as a profibrotic factor to promote pulmonary fibrogenesis. | Cell Death & Disease

Fig. 6: PICALM functioned as a profibrotic factor to promote pulmonary fibrogenesis.

From: YTHDC1 phase separation drives the nuclear export of m6A-modified lncNONMMUT062668.2 through the transport complex SRSF3–ALYREF–XPO5 to aggravate pulmonary fibrosis

Fig. 6

a Immunofluorescence images revealed that PICALM expression increased in the nucleus and cytoplasm under the TGF-β1 or PICALM overexpression treatment and decreased under the si-PICALM treatment. b COL1A, COL3A, VIM, α-SMA, and PICALM expression levels increased with the prolongation of the time of TGF-β1 action. c Western blot unveiled that PICALM, COL1A, COL3A, FAP, VIM, and α-SMA expression levels were decreased by si-PICALM and increased by PICALM overexpression. d IncuCyte S3 live-cell analysis confirmed that myofibroblast proliferation was inhibited by si-PICALM and promoted by PICALM overexpression. e Scratch assays confirmed that si-PICALM reduced cell migration, whereas PICALM overexpression enhanced cell migration.

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