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The role of type 1 pericyte in the differentiation to beige adipocytes in NG2-CREERTM and R26RRFP mice with cancer-associated cachexia

Grant number: 19/13982-2
Support Opportunities:Scholarships in Brazil - Scientific Initiation
Start date: March 01, 2020
End date: December 31, 2020
Field of knowledge:Biological Sciences - Physiology - Physiology of Organs and Systems
Principal Investigator:Miguel Luiz Batista Junior
Grantee:Ana Júlia de Oliveira Machado
Host Institution: Pró-Reitoria Acadêmica. Universidade de Mogi das Cruzes (UMC). Campus da Sede Mogi das Cruzes. Mogi das Cruzes , SP, Brazil

Abstract

Cachexia is a multifactorial syndrome characterized by continuous reduction of total body mass that cannot be fully reversed by nutritional support. This syndrome leads to progressive functional impairment and mainly affects skeletal muscle and adipose tissue (AT). In the development of cachexia, AT is affected early, being an endocrine organ constituted of several cell types, including, white adipocytes, brown adipocytes, adipocytes beges, pericytes, precursor cells of adipocytes, among others. The accumulation of beige adipocytes in white adipose tissue (WAT) is known as browning, a process induced according to thermogenic need. Cachexia is able to induce browning in WAT, with an accentuated reduction in body mass, especially of AT and skeletal muscle. Adipocytes, depending on the conditions of the internal environment, are derived from multipotent mesenchymal stem cells (MSC) that have the ability to differentiate and generate several cell lines. Studies have shown that MSC differentiate into adipocytes. However, it is unknown whether during the browning process, induced by cancer-associated cachexia, precursor MSC of type 1 pericytes are recruited to differentiate into beige adipocytes. Therefore, the objective of this project is to evaluate the potential differentiation of precursors of type 1 pericytes in beige adipocytes induced by cancer-associated cachexia through the crossing of NG2-CreERTM and R26RRFP mice.

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