MiR155 deficiency aggravates high-fat diet-induced adipose tissue fibrosis in male mice

Kandy T. Velázquez, Reilly T. Enos, Meredith S. Carson, Taryn L. Cranford, Jackie E. Bader, Alexander T. Sougiannis, Cara Pritchett, Daping Fan, James Carson, E. Angela Murphy

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Abstract

Noncoding RNAs are emerging as regulators of inflammatory and metabolic processes. There is evidence to suggest that miRNA155 (miR155) may be linked to inflammation and processes associated with adipogenesis. We examined the impact of global miRNA-155 deletion (miR155 -/- ) on the development of high-fat diet (HFD)-induced obesity. We hypothesized that loss of miR155 would decrease adipose tissue inflammation and improve the metabolic profile following HFD feedings. Beginning at 4-5 weeks of age, male miR155 -/- and wild-type (WT) mice (n = 13-14) on a C57BL/6 background were fed either a HFD or low-fat diet for 20 weeks. Body weight was monitored throughout the study. Baseline and terminal body composition was assessed by DEXA analysis. Adipose tissue mRNA expression (RTqPCR) of macrophage markers (F4/80, CD11c, and CD206) and inflammatory mediators (MCP-1 and TNF-α) as well as adiponectin were measured along with activation of NFjB-p65 and JNK and PPAR-λ. Adipose tissue fibrosis was assessed by picrosirius red staining and western blot analysis of Collagen I, III, and VI. Glucose metabolism and insulin resistance were assessed by Homeostatic Model Assessment - Insulin Resistance (HOMAIR), and a glucose tolerance test. Compared to WT HFD mice, miR155 -/- HFD mice displayed similar body weights, yet reduced visceral adipose tissue accumulation. However, miR155 -/- HFD displayed exacerbated adipose tissue fibrosis and decreased PPAR-λ protein content. The loss of miR155 did not affect adipose tissue inflammation or glucose metabolism. In conclusion, miR155 deletion did not attenuate the development of the obese phenotype, but adipose tissue fibrosis was exacerbated, possibly through changes to adipogenic processes.

Original languageEnglish (US)
Article numbere13412
JournalPhysiological Reports
Volume5
Issue number18
DOIs
StatePublished - Sep 1 2017

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High Fat Diet
Adipose Tissue
Fibrosis
Peroxisome Proliferator-Activated Receptors
Inflammation
Insulin Resistance
Body Weight
Glucose
Adipogenesis
Untranslated RNA
Fat-Restricted Diet
Metabolome
Intra-Abdominal Fat
Adiponectin
Glucose Tolerance Test
Body Composition
MicroRNAs
Collagen
Obesity
Western Blotting

All Science Journal Classification (ASJC) codes

  • Physiology
  • Physiology (medical)

Cite this

Velázquez, K. T., Enos, R. T., Carson, M. S., Cranford, T. L., Bader, J. E., Sougiannis, A. T., ... Murphy, E. A. (2017). MiR155 deficiency aggravates high-fat diet-induced adipose tissue fibrosis in male mice. Physiological Reports, 5(18), [e13412]. https://doi.org/10.14814/phy2.13412

MiR155 deficiency aggravates high-fat diet-induced adipose tissue fibrosis in male mice. / Velázquez, Kandy T.; Enos, Reilly T.; Carson, Meredith S.; Cranford, Taryn L.; Bader, Jackie E.; Sougiannis, Alexander T.; Pritchett, Cara; Fan, Daping; Carson, James; Murphy, E. Angela.

In: Physiological Reports, Vol. 5, No. 18, e13412, 01.09.2017.

Research output: Contribution to journalArticle

Velázquez, KT, Enos, RT, Carson, MS, Cranford, TL, Bader, JE, Sougiannis, AT, Pritchett, C, Fan, D, Carson, J & Murphy, EA 2017, 'MiR155 deficiency aggravates high-fat diet-induced adipose tissue fibrosis in male mice', Physiological Reports, vol. 5, no. 18, e13412. https://doi.org/10.14814/phy2.13412
Velázquez KT, Enos RT, Carson MS, Cranford TL, Bader JE, Sougiannis AT et al. MiR155 deficiency aggravates high-fat diet-induced adipose tissue fibrosis in male mice. Physiological Reports. 2017 Sep 1;5(18). e13412. https://doi.org/10.14814/phy2.13412
Velázquez, Kandy T. ; Enos, Reilly T. ; Carson, Meredith S. ; Cranford, Taryn L. ; Bader, Jackie E. ; Sougiannis, Alexander T. ; Pritchett, Cara ; Fan, Daping ; Carson, James ; Murphy, E. Angela. / MiR155 deficiency aggravates high-fat diet-induced adipose tissue fibrosis in male mice. In: Physiological Reports. 2017 ; Vol. 5, No. 18.
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