Matches in SemOpenAlex for { <https://semopenalex.org/work/W4377029477> ?p ?o ?g. }
Showing items 1 to 63 of
63
with 100 items per page.
- W4377029477 abstract "<b>Abstract ID 19127</b> <b>Poster Board 306</b> Cardiomyocytes are known to secrete signaling factors that can communicate with other organ systems, particularly in response to cardiometabolic stressors such as obesity. Under conditions of cardiometabolic stress, the expression and activity of cardiac GPCR kinase 2 (GRK2), which regulates β-adrenergic receptors in the heart, is upregulated. Previously we have shown that cardiac signaling factors alter adiposity in mice fed a high fat diet, and specific metabolic responses in adipose tissue are dependent on cardiac GRK2 levels and activity. However, the mechanisms responsible for this are unknown. We hypothesize that signaling factors secreted from the heart mediate adiposity and the development of cardiometabolic disease and are regulated by GRK2. To test this, conditioned media from control and GRK2 overexpressing neonatal rat ventricular myocytes (NRVM) was collected and applied to 3T3-L1 adipocytes. 3T3-L1 cells were then assessed by BODIPY fluorescent imaging, protein immunoblotting and qPCR. NRVM conditioned media was also analyzed by mass spectrometry to identify potential signaling factors. Conditioned media treated 3T3-L1 adipocytes demonstrated reduced lipid accumulation and adipogenic marker expression. Conditioned media from GRK2 overexpressing NRVMs further decreased lipid accumulation and differentiation in 3T3-L1 adipocytes. Proteomic analysis of conditioned media revealed several proteins with adipocyte regulatory roles. These findings indicate that cardiomyocyte-released signaling factors influence adipocyte differentiation that is further enhanced by GRK2 overexpression. Future work aims to identify the specific factors responsible and whether these may be from cardiac secreted exosomes. These findings will be used to elucidate novel mechanisms involved in heart-fat communication and cardiometabolic disease development. This research was funded by NIH R01 HL061690, NIH P01 HL134608 and AHA 18MERIT33900036." @default.
- W4377029477 created "2023-05-19" @default.
- W4377029477 creator A5022501132 @default.
- W4377029477 creator A5062462804 @default.
- W4377029477 creator A5075648082 @default.
- W4377029477 creator A5085580608 @default.
- W4377029477 date "2023-05-18" @default.
- W4377029477 modified "2023-09-29" @default.
- W4377029477 title "Cardiomyocyte Signaling Factors are Responsible for Heart-Fat Communication and Mediate the Development of Cardiometabolic Disease" @default.
- W4377029477 doi "https://doi.org/10.1124/jpet.122.191270" @default.
- W4377029477 hasPublicationYear "2023" @default.
- W4377029477 type Work @default.
- W4377029477 citedByCount "0" @default.
- W4377029477 crossrefType "proceedings-article" @default.
- W4377029477 hasAuthorship W4377029477A5022501132 @default.
- W4377029477 hasAuthorship W4377029477A5062462804 @default.
- W4377029477 hasAuthorship W4377029477A5075648082 @default.
- W4377029477 hasAuthorship W4377029477A5085580608 @default.
- W4377029477 hasBestOaLocation W43770294771 @default.
- W4377029477 hasConcept C122927707 @default.
- W4377029477 hasConcept C126322002 @default.
- W4377029477 hasConcept C134018914 @default.
- W4377029477 hasConcept C135285700 @default.
- W4377029477 hasConcept C142536801 @default.
- W4377029477 hasConcept C150555746 @default.
- W4377029477 hasConcept C170493617 @default.
- W4377029477 hasConcept C171089720 @default.
- W4377029477 hasConcept C2776175234 @default.
- W4377029477 hasConcept C62478195 @default.
- W4377029477 hasConcept C71924100 @default.
- W4377029477 hasConcept C78976303 @default.
- W4377029477 hasConcept C86803240 @default.
- W4377029477 hasConcept C95444343 @default.
- W4377029477 hasConceptScore W4377029477C122927707 @default.
- W4377029477 hasConceptScore W4377029477C126322002 @default.
- W4377029477 hasConceptScore W4377029477C134018914 @default.
- W4377029477 hasConceptScore W4377029477C135285700 @default.
- W4377029477 hasConceptScore W4377029477C142536801 @default.
- W4377029477 hasConceptScore W4377029477C150555746 @default.
- W4377029477 hasConceptScore W4377029477C170493617 @default.
- W4377029477 hasConceptScore W4377029477C171089720 @default.
- W4377029477 hasConceptScore W4377029477C2776175234 @default.
- W4377029477 hasConceptScore W4377029477C62478195 @default.
- W4377029477 hasConceptScore W4377029477C71924100 @default.
- W4377029477 hasConceptScore W4377029477C78976303 @default.
- W4377029477 hasConceptScore W4377029477C86803240 @default.
- W4377029477 hasConceptScore W4377029477C95444343 @default.
- W4377029477 hasLocation W43770294771 @default.
- W4377029477 hasOpenAccess W4377029477 @default.
- W4377029477 hasPrimaryLocation W43770294771 @default.
- W4377029477 hasRelatedWork W2017606817 @default.
- W4377029477 hasRelatedWork W2027098794 @default.
- W4377029477 hasRelatedWork W2048359366 @default.
- W4377029477 hasRelatedWork W2065069836 @default.
- W4377029477 hasRelatedWork W2118746168 @default.
- W4377029477 hasRelatedWork W2125103862 @default.
- W4377029477 hasRelatedWork W2228231544 @default.
- W4377029477 hasRelatedWork W2547949331 @default.
- W4377029477 hasRelatedWork W2906294792 @default.
- W4377029477 hasRelatedWork W2998970372 @default.
- W4377029477 isParatext "false" @default.
- W4377029477 isRetracted "false" @default.
- W4377029477 workType "article" @default.