Abstract
BackgroundPerivascular adipose tissue (PVAT) regulates function and remodeling of its adjacent arteries via paracrine actions of adipocyte‐derived factors. The vasoactive effects of PVAT are vascular bed specific and the morphology and function of perivascular adipocytes differs from adipocytes of other adipose depots. In normal pregnancy, there is an increase in circulating adipokines, expansion and inflammation of non‐perivascular adipose tissue; however, the metabolic and inflammatory profiles of PVAT have not been defined. In addition, in normal pregnancy, extensive uterine artery remodeling and increased vasodilatory responses contribute to increased uterine blood flow. Whether uterine PVAT plays a role in these adaptations is currently unknown. Thus, our goals are to define the metabolic and inflammatory profiles of uterine PVAT, and examine its vasoactive effects during pregnancy.HypothesisIn normal pregnancy, uterine PVAT would have increased inflammation and modulate uterine artery reactivity.MethodsUterine PVAT, mesenteric and uterine arteries from pregnant (gestational day 16, term=22–23) and aged‐matched non‐pregnant rats were used. To determine gene and protein expression of adipokines in uterine PVAT, we used reverse transcription polymerase chain reaction (RT‐PCR) and a proteome adipokine profiler, respectively. Circulating leptin and adiponectin concentrations were determined using ELISA. To evaluate the vasoactive effects of uterine PVAT on uterine artery function, we measured uterine and mesenteric artery reactivity in the presence and absence of uterine PVAT using wire myography.ResultsGene expression of interleukin (IL)‐11, and monocyte chemoattractant protein‐1 (MCP‐1) were upregulated in uterine PVAT from pregnant rats by 4.8‐ and 2.8‐fold, respectively, as compared to non‐pregnant rats. Protein expression of these adipocytokines as well as expression of IL‐6 and IL‐10 were also greater in uterine PVAT from pregnant compared to non‐pregnant rats. While mRNA expression of leptin receptor, OB‐Rb, did not change with pregnancy, leptin gene expression was downregulated by 1.7‐fold. Pregnancy did not affect mRNA expression of adiponectin and its receptor, Adipo‐R1, in uterine PVAT. Leptin (112.6 ± 10.7 pg/ml vs. 251.0 ± 25.8 pg/ml) and adiponectin (17561 ± 1460 ng/ml vs. 25564 ± 2950 ng/ml) concentrations were greater in sera from pregnant compared to non‐pregnant rats (p≤0.02). Uterine arteries from pregnant rats incubated with PVAT had increased contractile responses to potassium chloride [KCl (30 mM), PVAT(−): 4.0 ± 0.8 mN vs. PVAT(+): 14.7 ± 1.7 mN, p<0.05]. To establish whether the vasoactive effects of uterine PVAT are vascular bed specific, mesenteric arteries from pregnant rats were incubated with uterine PVAT. Arteries incubated with uterine PVAT had increased contractile responses to KCl [area under the curve, PVAT(−): 366 ± 46 vs. PVAT(+): 529 ± 53, p=0.02].ConclusionPregnancy upregulates inflammation, alters expression of adipokines and their receptors, and promotes a pro‐contractile profile in uterine PVAT.Support or Funding InformationUNT Health Science Center Pilot Grant.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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