Proliferative, Migratory, and Transition Properties Reveal Metastate of Human Amnion Cells

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

Amnion epithelial cell (AEC) shedding causes microfractures in human placental membranes during gestation. However, microfractures are healed to maintain membrane integrity. To better understand the cellular mechanisms of healing and tissue remodeling, scratch assays were performed using primary AECs derived from normal term not in labor membranes. AECs were grown under different conditions: i) normal cultures (control), ii) oxidative stress (OS) induction by cigarette smoke extract (CSE), iii) co-treatment of CSE and antioxidant N-acetyl-L-cysteine, and iv) treatment with amniotic fluid (AF). Cell migration time and distance, changes in intermediate filament (cytokeratin-18 and vimentin) expressions, and cellular senescence were determined. Control AECs in culture exhibited a metastate with the expression of both cytokeratin-18 and vimentin. During healing, AECs proliferated, migrated, and transitioned from epithelial to mesenchymal phenotype with increased vimentin. Wound healing was associated with mesenchymal to epithelial transition (MET). CSE-induced OS and senescence prevented wound healing in which cells sustained mesenchymal state. N-acetyl-L-cysteine reversed CSE's effect to aid wound closure through MET. AF accelerated cellular transitions and healing. Our data suggest that AECs undergo epithelial to mesenchymal transition during proliferation and migration and MET at the injury site to promote healing. AF accelerated whereas OS diminished cellular transitions and healing. OS-inducing pregnancy risk factors may diminish remodeling capacity contributing to membrane dysfunction, leading to preterm birth.

Original languageEnglish (US)
Pages (from-to)2004-2015
Number of pages12
JournalAmerican Journal of Pathology
Volume188
Issue number9
DOIs
StatePublished - Sep 1 2018

Fingerprint

Amnion
Epithelial-Mesenchymal Transition
Oxidative Stress
Vimentin
Amniotic Fluid
Smoke
Tobacco Products
Keratin-18
Stress Fractures
Membranes
Acetylcysteine
Wound Healing
Pregnancy
Intermediate Filaments
Cell Aging
Premature Birth
Wounds and Injuries
Cell Movement
Antioxidants
Epithelial Cells

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Proliferative, Migratory, and Transition Properties Reveal Metastate of Human Amnion Cells. / Richardson, Lauren; Menon, Ramkumar.

In: American Journal of Pathology, Vol. 188, No. 9, 01.09.2018, p. 2004-2015.

Research output: Contribution to journalArticle

@article{0d221667b84d4081a7b26dbfdd910f95,
title = "Proliferative, Migratory, and Transition Properties Reveal Metastate of Human Amnion Cells",
abstract = "Amnion epithelial cell (AEC) shedding causes microfractures in human placental membranes during gestation. However, microfractures are healed to maintain membrane integrity. To better understand the cellular mechanisms of healing and tissue remodeling, scratch assays were performed using primary AECs derived from normal term not in labor membranes. AECs were grown under different conditions: i) normal cultures (control), ii) oxidative stress (OS) induction by cigarette smoke extract (CSE), iii) co-treatment of CSE and antioxidant N-acetyl-L-cysteine, and iv) treatment with amniotic fluid (AF). Cell migration time and distance, changes in intermediate filament (cytokeratin-18 and vimentin) expressions, and cellular senescence were determined. Control AECs in culture exhibited a metastate with the expression of both cytokeratin-18 and vimentin. During healing, AECs proliferated, migrated, and transitioned from epithelial to mesenchymal phenotype with increased vimentin. Wound healing was associated with mesenchymal to epithelial transition (MET). CSE-induced OS and senescence prevented wound healing in which cells sustained mesenchymal state. N-acetyl-L-cysteine reversed CSE's effect to aid wound closure through MET. AF accelerated cellular transitions and healing. Our data suggest that AECs undergo epithelial to mesenchymal transition during proliferation and migration and MET at the injury site to promote healing. AF accelerated whereas OS diminished cellular transitions and healing. OS-inducing pregnancy risk factors may diminish remodeling capacity contributing to membrane dysfunction, leading to preterm birth.",
author = "Lauren Richardson and Ramkumar Menon",
year = "2018",
month = "9",
day = "1",
doi = "10.1016/j.ajpath.2018.05.019",
language = "English (US)",
volume = "188",
pages = "2004--2015",
journal = "American Journal of Pathology",
issn = "0002-9440",
publisher = "Elsevier Inc.",
number = "9",

}

TY - JOUR

T1 - Proliferative, Migratory, and Transition Properties Reveal Metastate of Human Amnion Cells

AU - Richardson, Lauren

AU - Menon, Ramkumar

PY - 2018/9/1

Y1 - 2018/9/1

N2 - Amnion epithelial cell (AEC) shedding causes microfractures in human placental membranes during gestation. However, microfractures are healed to maintain membrane integrity. To better understand the cellular mechanisms of healing and tissue remodeling, scratch assays were performed using primary AECs derived from normal term not in labor membranes. AECs were grown under different conditions: i) normal cultures (control), ii) oxidative stress (OS) induction by cigarette smoke extract (CSE), iii) co-treatment of CSE and antioxidant N-acetyl-L-cysteine, and iv) treatment with amniotic fluid (AF). Cell migration time and distance, changes in intermediate filament (cytokeratin-18 and vimentin) expressions, and cellular senescence were determined. Control AECs in culture exhibited a metastate with the expression of both cytokeratin-18 and vimentin. During healing, AECs proliferated, migrated, and transitioned from epithelial to mesenchymal phenotype with increased vimentin. Wound healing was associated with mesenchymal to epithelial transition (MET). CSE-induced OS and senescence prevented wound healing in which cells sustained mesenchymal state. N-acetyl-L-cysteine reversed CSE's effect to aid wound closure through MET. AF accelerated cellular transitions and healing. Our data suggest that AECs undergo epithelial to mesenchymal transition during proliferation and migration and MET at the injury site to promote healing. AF accelerated whereas OS diminished cellular transitions and healing. OS-inducing pregnancy risk factors may diminish remodeling capacity contributing to membrane dysfunction, leading to preterm birth.

AB - Amnion epithelial cell (AEC) shedding causes microfractures in human placental membranes during gestation. However, microfractures are healed to maintain membrane integrity. To better understand the cellular mechanisms of healing and tissue remodeling, scratch assays were performed using primary AECs derived from normal term not in labor membranes. AECs were grown under different conditions: i) normal cultures (control), ii) oxidative stress (OS) induction by cigarette smoke extract (CSE), iii) co-treatment of CSE and antioxidant N-acetyl-L-cysteine, and iv) treatment with amniotic fluid (AF). Cell migration time and distance, changes in intermediate filament (cytokeratin-18 and vimentin) expressions, and cellular senescence were determined. Control AECs in culture exhibited a metastate with the expression of both cytokeratin-18 and vimentin. During healing, AECs proliferated, migrated, and transitioned from epithelial to mesenchymal phenotype with increased vimentin. Wound healing was associated with mesenchymal to epithelial transition (MET). CSE-induced OS and senescence prevented wound healing in which cells sustained mesenchymal state. N-acetyl-L-cysteine reversed CSE's effect to aid wound closure through MET. AF accelerated cellular transitions and healing. Our data suggest that AECs undergo epithelial to mesenchymal transition during proliferation and migration and MET at the injury site to promote healing. AF accelerated whereas OS diminished cellular transitions and healing. OS-inducing pregnancy risk factors may diminish remodeling capacity contributing to membrane dysfunction, leading to preterm birth.

UR - http://www.scopus.com/inward/record.url?scp=85051386118&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85051386118&partnerID=8YFLogxK

U2 - 10.1016/j.ajpath.2018.05.019

DO - 10.1016/j.ajpath.2018.05.019

M3 - Article

C2 - 29981743

AN - SCOPUS:85051386118

VL - 188

SP - 2004

EP - 2015

JO - American Journal of Pathology

JF - American Journal of Pathology

SN - 0002-9440

IS - 9

ER -