Hypoxia primed placental mesenchymal stem cells for wound healing

Suja Ann Mathew, Bhawna Chandravanshi, Ramesh Bhonde

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

Aims To investigate how Placental Mesenchymal Stem Cells (P-MSCs) would adapt themselves and survive under hypoxic conditions which are prevalent in most injury sites. Main methods P-MSCs were isolated from term placenta and characterised under normoxia and hypoxia (2–2.5% O2). Cells were examined for morphology and surface marker variations by flow cytometry analysis. Glucose stimulated insulin secretion was assayed by Insulin ELISA Kit. Gene expression levels were estimated using Real Time PCR for hypoxia inducible factor1 alpha, Insulin (INS), Glucose transporters (GLUT-1, GLUT-2 and GLUT-3), Adhesion Proteins- Integrins, Fibronectin1 (FN1), E-Cadherin (CDH1), and N-Cadherin (CDH2) and angiogenesis marker VEGFA. Immunofluorescence assay was done to confirm the presence of C-Peptide, GLUT 2, E-Cadherin and ITGB3. Adhesion was confirmed assessed on fibronectin binding. Key findings We show that insulin secretion is not hampered under hypoxia. We found an upregulation of glucose transporters under hypoxia indicating enhanced glucose uptake needed to cater to metabolic demands of proliferating cells. Up regulation of adhesion molecules was seen under hypoxia indicative of a favoured environment for retention of cells at the injury site. We also found increased level of angiogenesis of P-MSCs under hypoxia. Significance Our present study thus demonstrates for the first time that P-MSCs modulate themselves under hypoxic conditions by secreting insulin, up regulating glucose transporters and adhesion molecules and eventually exhibiting an increased angiogenic potential. We thus infer that priming P-MSCs under hypoxia, could make them more suitable for wound healing applications.

Original languageEnglish
Pages (from-to)85-92
Number of pages8
JournalLife Sciences
Volume182
DOIs
Publication statusPublished - 01-08-2017

Fingerprint

Stem cells
Mesenchymal Stromal Cells
Wound Healing
Facilitative Glucose Transport Proteins
Insulin
Cadherins
Adhesion
Cell Hypoxia
Glucose Transporter Type 3
Up-Regulation
Glucose
Molecules
Flow cytometry
C-Peptide
Wounds and Injuries
Fibronectins
Gene expression
Integrins
Placenta
Fluorescent Antibody Technique

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

Mathew, Suja Ann ; Chandravanshi, Bhawna ; Bhonde, Ramesh. / Hypoxia primed placental mesenchymal stem cells for wound healing. In: Life Sciences. 2017 ; Vol. 182. pp. 85-92.
@article{1dfa61ba8a624d638ffd0a925981e09a,
title = "Hypoxia primed placental mesenchymal stem cells for wound healing",
abstract = "Aims To investigate how Placental Mesenchymal Stem Cells (P-MSCs) would adapt themselves and survive under hypoxic conditions which are prevalent in most injury sites. Main methods P-MSCs were isolated from term placenta and characterised under normoxia and hypoxia (2–2.5{\%} O2). Cells were examined for morphology and surface marker variations by flow cytometry analysis. Glucose stimulated insulin secretion was assayed by Insulin ELISA Kit. Gene expression levels were estimated using Real Time PCR for hypoxia inducible factor1 alpha, Insulin (INS), Glucose transporters (GLUT-1, GLUT-2 and GLUT-3), Adhesion Proteins- Integrins, Fibronectin1 (FN1), E-Cadherin (CDH1), and N-Cadherin (CDH2) and angiogenesis marker VEGFA. Immunofluorescence assay was done to confirm the presence of C-Peptide, GLUT 2, E-Cadherin and ITGB3. Adhesion was confirmed assessed on fibronectin binding. Key findings We show that insulin secretion is not hampered under hypoxia. We found an upregulation of glucose transporters under hypoxia indicating enhanced glucose uptake needed to cater to metabolic demands of proliferating cells. Up regulation of adhesion molecules was seen under hypoxia indicative of a favoured environment for retention of cells at the injury site. We also found increased level of angiogenesis of P-MSCs under hypoxia. Significance Our present study thus demonstrates for the first time that P-MSCs modulate themselves under hypoxic conditions by secreting insulin, up regulating glucose transporters and adhesion molecules and eventually exhibiting an increased angiogenic potential. We thus infer that priming P-MSCs under hypoxia, could make them more suitable for wound healing applications.",
author = "Mathew, {Suja Ann} and Bhawna Chandravanshi and Ramesh Bhonde",
year = "2017",
month = "8",
day = "1",
doi = "10.1016/j.lfs.2017.06.016",
language = "English",
volume = "182",
pages = "85--92",
journal = "Life Sciences",
issn = "0024-3205",
publisher = "Elsevier Inc.",

}

Hypoxia primed placental mesenchymal stem cells for wound healing. / Mathew, Suja Ann; Chandravanshi, Bhawna; Bhonde, Ramesh.

In: Life Sciences, Vol. 182, 01.08.2017, p. 85-92.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Hypoxia primed placental mesenchymal stem cells for wound healing

AU - Mathew, Suja Ann

AU - Chandravanshi, Bhawna

AU - Bhonde, Ramesh

PY - 2017/8/1

Y1 - 2017/8/1

N2 - Aims To investigate how Placental Mesenchymal Stem Cells (P-MSCs) would adapt themselves and survive under hypoxic conditions which are prevalent in most injury sites. Main methods P-MSCs were isolated from term placenta and characterised under normoxia and hypoxia (2–2.5% O2). Cells were examined for morphology and surface marker variations by flow cytometry analysis. Glucose stimulated insulin secretion was assayed by Insulin ELISA Kit. Gene expression levels were estimated using Real Time PCR for hypoxia inducible factor1 alpha, Insulin (INS), Glucose transporters (GLUT-1, GLUT-2 and GLUT-3), Adhesion Proteins- Integrins, Fibronectin1 (FN1), E-Cadherin (CDH1), and N-Cadherin (CDH2) and angiogenesis marker VEGFA. Immunofluorescence assay was done to confirm the presence of C-Peptide, GLUT 2, E-Cadherin and ITGB3. Adhesion was confirmed assessed on fibronectin binding. Key findings We show that insulin secretion is not hampered under hypoxia. We found an upregulation of glucose transporters under hypoxia indicating enhanced glucose uptake needed to cater to metabolic demands of proliferating cells. Up regulation of adhesion molecules was seen under hypoxia indicative of a favoured environment for retention of cells at the injury site. We also found increased level of angiogenesis of P-MSCs under hypoxia. Significance Our present study thus demonstrates for the first time that P-MSCs modulate themselves under hypoxic conditions by secreting insulin, up regulating glucose transporters and adhesion molecules and eventually exhibiting an increased angiogenic potential. We thus infer that priming P-MSCs under hypoxia, could make them more suitable for wound healing applications.

AB - Aims To investigate how Placental Mesenchymal Stem Cells (P-MSCs) would adapt themselves and survive under hypoxic conditions which are prevalent in most injury sites. Main methods P-MSCs were isolated from term placenta and characterised under normoxia and hypoxia (2–2.5% O2). Cells were examined for morphology and surface marker variations by flow cytometry analysis. Glucose stimulated insulin secretion was assayed by Insulin ELISA Kit. Gene expression levels were estimated using Real Time PCR for hypoxia inducible factor1 alpha, Insulin (INS), Glucose transporters (GLUT-1, GLUT-2 and GLUT-3), Adhesion Proteins- Integrins, Fibronectin1 (FN1), E-Cadherin (CDH1), and N-Cadherin (CDH2) and angiogenesis marker VEGFA. Immunofluorescence assay was done to confirm the presence of C-Peptide, GLUT 2, E-Cadherin and ITGB3. Adhesion was confirmed assessed on fibronectin binding. Key findings We show that insulin secretion is not hampered under hypoxia. We found an upregulation of glucose transporters under hypoxia indicating enhanced glucose uptake needed to cater to metabolic demands of proliferating cells. Up regulation of adhesion molecules was seen under hypoxia indicative of a favoured environment for retention of cells at the injury site. We also found increased level of angiogenesis of P-MSCs under hypoxia. Significance Our present study thus demonstrates for the first time that P-MSCs modulate themselves under hypoxic conditions by secreting insulin, up regulating glucose transporters and adhesion molecules and eventually exhibiting an increased angiogenic potential. We thus infer that priming P-MSCs under hypoxia, could make them more suitable for wound healing applications.

UR - http://www.scopus.com/inward/record.url?scp=85020883995&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85020883995&partnerID=8YFLogxK

U2 - 10.1016/j.lfs.2017.06.016

DO - 10.1016/j.lfs.2017.06.016

M3 - Article

C2 - 28625360

AN - SCOPUS:85020883995

VL - 182

SP - 85

EP - 92

JO - Life Sciences

JF - Life Sciences

SN - 0024-3205

ER -