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Methods: Early diabetes MDSCs and late diabetes MDSCs were respectively isolated from nearly normal young OZ rats and moderately hyperglycemic and severely dyslipidemic\/obese aged rats with erectile dysfunction. Monolayer cultures of early diabetic MDSCs were incubated 4 days in DMEM\/10% fetal calf serum\u00a0+ or\u00a0\u2212 aged OZ or lean Zucker serum from non-diabetic lean Zucker rats (0.5\u20135%) or with soluble palmitic acid (PA) (0.5\u20132 mM), cholesterol (CHOL) (50\u2013400 mg\/dL), or glucose (10\u201325 mM).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Main Outcome Measure<\/jats:title>\n                    <jats:p>Fat infiltration was estimated by Oil red O, apoptosis by TUNEL, protein expression by Western blots, and gene-GTS and microRNA (miR)-GTS were determined in these stem cells\u2019 RNA.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Aged OZ serum caused fat infiltration, apoptosis, myostatin overexpression, and impaired differentiation. Some of these changes, and also a proliferation decrease occurred with PA and CHOL. The gene-GTS changes by OZ serum did not resemble the in\u00a0vivo changes, but some occurred with PA and CHOL. The miR-GTS changes by OZ serum, PA, and CHOL resembled most of the in\u00a0vivo changes. Hyperglycemia did not replicate most alterations. Clinical Implications: MDSCs may be damaged in long-term UC-T2D\/obese patients and be ineffective in autologous human stem cell therapy, which may be prevented by excluding the damaged MDSCs.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Strength &amp; Limitations<\/jats:title>\n                    <jats:p>The in\u00a0vitro test of MDSCs is innovative and fast to define dyslipidemic factors inducing stem cell damage, its mechanism, prevention, and counteraction. Confirmation is required in other T2D\/obesity rat models and stem cells (including human), as well as miR-GTS biomarker validation as a stem cell damage biomarker.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Serum from long-term UC-T2D\/obese rats or dyslipidemic factors induces a noxious phenotype and miR-GTS on normal MDSCs, which may lead in\u00a0vivo to the repair inefficacy of late diabetic MDSCs. This suggests that autograft therapy with MDSCs in long-term UT-T2D obese patients may be ineffective, albeit this may be predictable by prior stem cell miR-GTS tests.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1016\/j.jsxm.2018.09.019","type":"journal-article","created":{"date-parts":[[2018,12,4]],"date-time":"2018-12-04T03:17:15Z","timestamp":1543893435000},"page":"1678-1697","update-policy":"https:\/\/doi.org\/10.1016\/elsevier_cm_policy","source":"Crossref","is-referenced-by-count":13,"title":["Dyslipidemia Is a Major Factor in Stem Cell Damage Induced by Uncontrolled Long-Term Type 2 Diabetes and Obesity in the Rat, as Suggested by the Effects on Stem Cell Culture"],"prefix":"10.1093","volume":"15","author":[{"given":"Maryam","family":"Masouminia","sequence":"first","affiliation":[{"name":"Division of Urology \u00a0 \u00a0 , Torrance, CA , USA"},{"name":"Department of Surgery \u00a0 \u00a0 , Torrance, CA , USA"},{"name":"Harbor-UCLA Medical Center and Los Angeles 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