Inhibition of stress-activated p38 mitogen-activated protein kinase induces low-density lipoprotein receptor expression.
We have recently shown that different signal transduction pathways initiated by a variety of agents converge on growth-responsive p42/44MAPK signaling cascade to induce low-density lipoprotein (LDL) receptor expression. Our recent demonstration that stress-activated p38MAPK negatively regulates LDL receptor expression in an isoform-specific manner via modulation of p42/44MAPK cascade represents a new dimension of complexity in the molecular communication that governs LDL receptor expression. The suggested one-way communication between p38MAPK and p42/44MAPK provides a potential mechanism for fine-tuning cellular levels of cholesterol in response to a diverse set of environmental cues, including stress. Cross talk between MAPKs opens new avenues toward understanding a variety of pathogenic processes; this makes them tempting targets for therapeutic interventions in cardiovascular diseases.
Mehta
K D
KD
Department of Biochemistry and Molecular Biology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock 72205, USA.
Miller
L
L
D000818:Animals; D017209:Apoptosis; D004789:Enzyme Activation; D006801:Humans; D006937:Hypercholesterolemia / Q000378:metabolism* / Q000503:physiopathology; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D011973:Receptors, LDL / Q000378:metabolism*; D015398:Signal Transduction; D013315:Stress, Psychological / Q000503:physiopathology; D048051:p38 Mitogen-Activated Protein Kinases
D011973:Receptors, LDL; D019950:Mitogen-Activated Protein Kinase 1; D020928:Mitogen-Activated Protein Kinases; D048051:p38 Mitogen-Activated Protein Kinases