Mechanical stress facilitates calcium influx and growth of alveolar epithelial cells via activation of the BDKRB1/Ca2+/CaMKII/MEK1/ERK axis DOI Creative Commons
Ying Zhang, Qingdong Zhang, Li Quan

et al.

Respiratory Research, Journal Year: 2025, Volume and Issue: 26(1)

Published: April 28, 2025

Mechanical stress and calcium metabolism are associated with lung development various pulmonary diseases. Our previous research demonstrated that BDKRB1/Ca2+ signal transduction may be involved in dysplasia resulting from scoliosis thoracic insufficiency. Therefore, the present study aims to investigate effects of mechanical on growth influx alveolar epithelial cells, as well role signaling these processes. Flow cytometry, CCK-8, EDU staining assay were employed assess cycle, influx, activity, proliferation RLE-6TN cells subjected stresses varying amplitudes (5%, 10% 15%). RT-qPCR western blotting performed evaluate BDKRB1/Ca2+/CaMKII/MEK1/ERK cells. at effectively enhanced viability, positive ratio, S-phase percentage, Ca2+ concentration while reducing G1-phase percentage. Conversely, 15% exerted an inhibitory effect cell proliferation. Additionally, significantly upregulated expression BDKRB1, CaMKIIα/δ, p-MEK1 p-ERK1/2 Notably, BDKRB1 knockdown attenuated stress-induced increase both Moreover, blocked activation Ca2⁺/CaMKII/MEK1/ERK pathway induced by stress. Appropriate levels contribute modulating signaling.

Language: Английский

Magnetically Stimulated Myogenesis Recruits a CRY2-TRPC1 Photosensitive Signaling Axis DOI Creative Commons
Jan Nikolas Iversen, Yee Kit Tai,

Kwan Yu Wu

et al.

Cells, Journal Year: 2025, Volume and Issue: 14(3), P. 231 - 231

Published: Feb. 6, 2025

The cryptochromes are flavoproteins that either individually or synergistically respond to light and magnetic field directionality as well implicated in circadian rhythm entrainment development. Single brief exposures (10 min) low energy (1.5 mT) pulsed electromagnetic fields (PEMFs) were previously shown enhance myogenesis by stimulating transient receptor potential canonical 1 (TRPC1)-mediated Ca2+ entry, whereby downwardly directed produced greater myogenic enhancement than upwardly fields. Here, we show growth the dark results myoblasts losing their sensitivity both exposure directionality. By contrast, overexpressing silencing cryptochrome regulator 2 (CRY2) enhances reduces PEMF responses, respectively, under conditions of ambient light. Reducing cellular flavin adenine dinucleotide (FAD) content riboflavin kinase (RFK) attenuated responsiveness PEMFs inhibited selectivity for direction. upregulation TRPC1 cell cycle regulatory proteins typically observed response was instead fields, darkness, shielding, CRY2 RFK. A physical interaction between detected using coimmunoprecipitation immunofluorescence, revealing co-translocation into nucleus after exposure. These implicate an identified TRPC1-dependent magnetotransduction cascade.

Language: Английский

Citations

0
Cisd2 ensures adequate ER-mitochondrial coupling, thereby critically supporting mitochondrial function in neurons DOI Creative Commons
Jens Loncke, Ian de Ridder,

Rita La Rovere

et al.

Research Square (Research Square), Journal Year: 2025, Volume and Issue: unknown

Published: March 26, 2025

Abstract Loss of CISD2, an iron-sulfur cluster transfer protein, results in type 2 Wolfram syndrome (WFS2), a disorder associated with severe impacts on pancreatic beta cell and neuronal functions. CISD2 has been implicated Ca2+ signaling but the molecular basis cellular consequences remain poorly understood. In this work, we demonstrate that Cisd2 intersects intracellular dynamics at different levels, including as interactor IP3Rs protein contributing to ER-mitochondrial tethering. As such, loss HeLa cells reduced without majorly impact cytosolic signaling. these cells, deficiency promotes autophagic flux, yet minimal mitochondrial function. However, studying iPSC-derived cortical neurons, relevant for WFS2, revealed glutamate-evoked responses cytosol mitochondria contact. Correlating profound changes handling, function (oxygen consumption rate, ATP production, potential maintenance) was severely declined, while flux increased. Overall, deficiencies further resilience CISD2-deficient neurons against stress CISD2-KO were highly susceptible staurosporine, death inducer. work is one first decipher handling disease-relevant models, thereby revealing unique dependence their health resilience.

Language: Английский

Citations

0
Mitochondria-organelle crosstalk in establishing compartmentalized metabolic homeostasis DOI
Brandon Chen, Costas A. Lyssiotis, Yatrik M. Shah

et al.

Molecular Cell, Journal Year: 2025, Volume and Issue: 85(8), P. 1487 - 1508

Published: April 1, 2025

Language: Английский

Citations

0
Mechanical stress facilitates calcium influx and growth of alveolar epithelial cells via activation of the BDKRB1/Ca2+/CaMKII/MEK1/ERK axis DOI Creative Commons
Ying Zhang, Qingdong Zhang, Li Quan

et al.

Respiratory Research, Journal Year: 2025, Volume and Issue: 26(1)

Published: April 28, 2025

Mechanical stress and calcium metabolism are associated with lung development various pulmonary diseases. Our previous research demonstrated that BDKRB1/Ca2+ signal transduction may be involved in dysplasia resulting from scoliosis thoracic insufficiency. Therefore, the present study aims to investigate effects of mechanical on growth influx alveolar epithelial cells, as well role signaling these processes. Flow cytometry, CCK-8, EDU staining assay were employed assess cycle, influx, activity, proliferation RLE-6TN cells subjected stresses varying amplitudes (5%, 10% 15%). RT-qPCR western blotting performed evaluate BDKRB1/Ca2+/CaMKII/MEK1/ERK cells. at effectively enhanced viability, positive ratio, S-phase percentage, Ca2+ concentration while reducing G1-phase percentage. Conversely, 15% exerted an inhibitory effect cell proliferation. Additionally, significantly upregulated expression BDKRB1, CaMKIIα/δ, p-MEK1 p-ERK1/2 Notably, BDKRB1 knockdown attenuated stress-induced increase both Moreover, blocked activation Ca2⁺/CaMKII/MEK1/ERK pathway induced by stress. Appropriate levels contribute modulating signaling.

Language: Английский

Citations

0