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Related Experiment Video

Updated: May 9, 2026

Isolation, Culture, and Adipogenic Induction of Stromal Vascular Fraction-derived Preadipocytes from Mouse Periaortic Adipose Tissue

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Published on: July 21, 2023

Rictor in perivascular adipose tissue controls vascular function by regulating inflammatory molecule expression.

Indranil Bhattacharya¹, Katja Drägert, Verena Albert

¹Research Unit, Division of Internal Medicine, University Hospital of Zurich, Zurich, Switzerland.

Arteriosclerosis, Thrombosis, and Vascular Biology

|July 23, 2013

Summary

Inactivating mammalian target of rapamycin complex 2 (mTORC2) in perivascular adipose tissue (PVAT) increases inflammation and impairs vascular function. Targeting mTORC2 in adipose tissue may treat vascular damage.

Keywords:

adipose tissue inflammation mammalian target of rapamycin complex 2 nitric oxide synthase type II perivascular adipose tissue thoracic aorta

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Area of Science:

Vascular Biology
Adipose Tissue Biology
Molecular Signaling

Background:

Perivascular adipose tissue (PVAT) influences blood vessel function through secreted molecules.
Mammalian target of rapamycin complex 2 (mTORC2) is involved in inflammation and present in adipose tissue.

Purpose of the Study:

To investigate the role of adipose-specific mTORC2 in regulating PVAT inflammation and vascular function.
To determine if deleting rictor, an mTORC2 component, in adipose tissue affects vascular tone.

Main Methods:

Generated mice with adipose-specific deletion of rictor (rictor(ad-/-)).
Assessed mTORC2 activity via Akt phosphorylation.
Performed ex vivo functional analysis of thoracic aortae.
Quantified inflammatory markers (cytokines, inducible nitric oxide synthase) in PVAT using qPCR and Bioplex.

Main Results:

Adipose-specific rictor deletion reduced Akt phosphorylation in PVAT.
Thoracic aortae from rictor(ad-/-) mice showed increased contraction and impaired dilation.
PVAT from rictor(ad-/-) mice exhibited elevated interleukin-6, macrophage inflammatory protein-1α, and tumor necrosis factor-α.
Inducible nitric oxide synthase expression was upregulated in PVAT, and its inhibition normalized vascular reactivity.

Conclusions:

mTORC2 is a key regulator of PVAT's protective role in maintaining normal vascular tone.
Modulating adipose tissue mTORC2 activity presents a potential therapeutic strategy for vascular damage linked to inflammation.