Red blood cells inhibit proliferation and stimulate apoptosis in human lung fibroblasts In vitro

K. Fredriksson, H. Stridh, J. Lundahl, S. I. Rennard, C. M. Skold

Research output: Contribution to journalArticle

12 Citations (Scopus)

Abstract

Cell proliferation and apoptosis are both important mechanisms for the regulation of tissue homeostasis. For instance, proliferation is crucial in wound repair, whereas apoptosis is important for removal of damaged cells and resolution of inflammation. Imbalance between cell proliferation and apoptosis can therefore lead to pathological conditions and disease. In inflammatory and fibrotic lung disorders, red blood cells (RBCs) can interact with fibroblasts and connective tissue. In the present study, we therefore hypothesized that the presence of RBCs can affect fibroblast proliferation and apoptosis. Human foetal lung fibroblasts (HFL-1) were cultured in the presence or absence of purified whole RBCs and RBC-conditioned media. RBC significantly decreased fibroblast proliferation as determined both by DNA content analysis (Hoechst 33258 staining, P<0.01; WST-1, P<0.001) and BrdU incorporation. After treatment with staurosporine (STS) for 48 h, apoptosis was determined by TUNEL and propidium iodide staining followed by flow cytometry analysis. RBCs augmented STS-induced apoptosis (median: 46.4%; range 12.0-90.4) compared to control cells (median 26.2%; range 7.1-45.5). Thus, our data indicate that the presence of RBCs affects both fibroblast proliferation and susceptibility to undergo apoptosis. Our findings therefore suggest a role for RBCs in regulating fibroblast homeostasis after tissue injury.

Original languageEnglish (US)
Pages (from-to)559-565
Number of pages7
JournalScandinavian Journal of Immunology
Volume59
Issue number6
DOIs
StatePublished - Jun 1 2004

Fingerprint

Fibroblasts
Erythrocytes
Cell Proliferation
Apoptosis
Lung
Staurosporine
Homeostasis
Staining and Labeling
Bisbenzimidazole
In Vitro Techniques
Propidium
In Situ Nick-End Labeling
Wounds and Injuries
Bromodeoxyuridine
Conditioned Culture Medium
Connective Tissue
Flow Cytometry
Inflammation
DNA

ASJC Scopus subject areas

  • Immunology

Cite this

Red blood cells inhibit proliferation and stimulate apoptosis in human lung fibroblasts In vitro. / Fredriksson, K.; Stridh, H.; Lundahl, J.; Rennard, S. I.; Skold, C. M.

In: Scandinavian Journal of Immunology, Vol. 59, No. 6, 01.06.2004, p. 559-565.

Research output: Contribution to journalArticle

Fredriksson, K. ; Stridh, H. ; Lundahl, J. ; Rennard, S. I. ; Skold, C. M. / Red blood cells inhibit proliferation and stimulate apoptosis in human lung fibroblasts In vitro. In: Scandinavian Journal of Immunology. 2004 ; Vol. 59, No. 6. pp. 559-565.
@article{4b38acb4dcc34710b070300c6d72cc79,
title = "Red blood cells inhibit proliferation and stimulate apoptosis in human lung fibroblasts In vitro",
abstract = "Cell proliferation and apoptosis are both important mechanisms for the regulation of tissue homeostasis. For instance, proliferation is crucial in wound repair, whereas apoptosis is important for removal of damaged cells and resolution of inflammation. Imbalance between cell proliferation and apoptosis can therefore lead to pathological conditions and disease. In inflammatory and fibrotic lung disorders, red blood cells (RBCs) can interact with fibroblasts and connective tissue. In the present study, we therefore hypothesized that the presence of RBCs can affect fibroblast proliferation and apoptosis. Human foetal lung fibroblasts (HFL-1) were cultured in the presence or absence of purified whole RBCs and RBC-conditioned media. RBC significantly decreased fibroblast proliferation as determined both by DNA content analysis (Hoechst 33258 staining, P<0.01; WST-1, P<0.001) and BrdU incorporation. After treatment with staurosporine (STS) for 48 h, apoptosis was determined by TUNEL and propidium iodide staining followed by flow cytometry analysis. RBCs augmented STS-induced apoptosis (median: 46.4{\%}; range 12.0-90.4) compared to control cells (median 26.2{\%}; range 7.1-45.5). Thus, our data indicate that the presence of RBCs affects both fibroblast proliferation and susceptibility to undergo apoptosis. Our findings therefore suggest a role for RBCs in regulating fibroblast homeostasis after tissue injury.",
author = "K. Fredriksson and H. Stridh and J. Lundahl and Rennard, {S. I.} and Skold, {C. M.}",
year = "2004",
month = "6",
day = "1",
doi = "10.1111/j.1365-3083.2004.01433.x",
language = "English (US)",
volume = "59",
pages = "559--565",
journal = "Scandinavian Journal of Immunology",
issn = "0300-9475",
publisher = "Wiley-Blackwell",
number = "6",

}

TY - JOUR

T1 - Red blood cells inhibit proliferation and stimulate apoptosis in human lung fibroblasts In vitro

AU - Fredriksson, K.

AU - Stridh, H.

AU - Lundahl, J.

AU - Rennard, S. I.

AU - Skold, C. M.

PY - 2004/6/1

Y1 - 2004/6/1

N2 - Cell proliferation and apoptosis are both important mechanisms for the regulation of tissue homeostasis. For instance, proliferation is crucial in wound repair, whereas apoptosis is important for removal of damaged cells and resolution of inflammation. Imbalance between cell proliferation and apoptosis can therefore lead to pathological conditions and disease. In inflammatory and fibrotic lung disorders, red blood cells (RBCs) can interact with fibroblasts and connective tissue. In the present study, we therefore hypothesized that the presence of RBCs can affect fibroblast proliferation and apoptosis. Human foetal lung fibroblasts (HFL-1) were cultured in the presence or absence of purified whole RBCs and RBC-conditioned media. RBC significantly decreased fibroblast proliferation as determined both by DNA content analysis (Hoechst 33258 staining, P<0.01; WST-1, P<0.001) and BrdU incorporation. After treatment with staurosporine (STS) for 48 h, apoptosis was determined by TUNEL and propidium iodide staining followed by flow cytometry analysis. RBCs augmented STS-induced apoptosis (median: 46.4%; range 12.0-90.4) compared to control cells (median 26.2%; range 7.1-45.5). Thus, our data indicate that the presence of RBCs affects both fibroblast proliferation and susceptibility to undergo apoptosis. Our findings therefore suggest a role for RBCs in regulating fibroblast homeostasis after tissue injury.

AB - Cell proliferation and apoptosis are both important mechanisms for the regulation of tissue homeostasis. For instance, proliferation is crucial in wound repair, whereas apoptosis is important for removal of damaged cells and resolution of inflammation. Imbalance between cell proliferation and apoptosis can therefore lead to pathological conditions and disease. In inflammatory and fibrotic lung disorders, red blood cells (RBCs) can interact with fibroblasts and connective tissue. In the present study, we therefore hypothesized that the presence of RBCs can affect fibroblast proliferation and apoptosis. Human foetal lung fibroblasts (HFL-1) were cultured in the presence or absence of purified whole RBCs and RBC-conditioned media. RBC significantly decreased fibroblast proliferation as determined both by DNA content analysis (Hoechst 33258 staining, P<0.01; WST-1, P<0.001) and BrdU incorporation. After treatment with staurosporine (STS) for 48 h, apoptosis was determined by TUNEL and propidium iodide staining followed by flow cytometry analysis. RBCs augmented STS-induced apoptosis (median: 46.4%; range 12.0-90.4) compared to control cells (median 26.2%; range 7.1-45.5). Thus, our data indicate that the presence of RBCs affects both fibroblast proliferation and susceptibility to undergo apoptosis. Our findings therefore suggest a role for RBCs in regulating fibroblast homeostasis after tissue injury.

UR - http://www.scopus.com/inward/record.url?scp=2942722511&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=2942722511&partnerID=8YFLogxK

U2 - 10.1111/j.1365-3083.2004.01433.x

DO - 10.1111/j.1365-3083.2004.01433.x

M3 - Article

C2 - 15182251

AN - SCOPUS:2942722511

VL - 59

SP - 559

EP - 565

JO - Scandinavian Journal of Immunology

JF - Scandinavian Journal of Immunology

SN - 0300-9475

IS - 6

ER -