Cellular origins of fibroblasts

Possible implications for organ fibrosis in systemic sclerosis

Arnold Postlethwaite, Hidenobu Shigemitsu, Siva Kanangat

Research output: Contribution to journalReview article

124 Citations (Scopus)

Abstract

Purpose of review: There is an intense interest in the potential of circulating blood cells and epithelium-related nonfibroblast cells to change into matrix synthesizing fibroblasts and myofibroblasts. These sources of fibroblasts may have importance in systemic sclerosis (scleroderma). Recent findings: Epithelial cells from different sources can transition into fibroblasts and myofibroblasts in response to transforming growth factor β and other growth factors/cytokines. This is called epithelial-mesenchymal transition (EMT). EMT has been repeatedly demonstrated to occur in several models of renal fibrosis including lupus prone mice. Quite unexpectedly, bone morphogenic protein 7 prevents EMT and protects lupus mice and other renal fibrosis models from developing fibrosis in the kidneys. Human peripheral blood mononuclear cells under different conditions of culture give rise to several different types of fibroblast-like cells. In SSc, it has been observed that the sera have low levels of serum amyloid protein. Serum amyloid protein has been found to inhibit the generation of fibrocytes from CD14+ precursors. The implications of these potential sources of fibroblasts and myofibroblasts in systemic sclerosis and related rheumatic diseases are discussed. Summary: Fibroblasts and myofibroblasts in skin and internal organs of patients with systemic sclerosis and related diseases may possibly arise not only from the resident fibroblast population but from epithelial cells, pericytes, monocytes, and other progenitors from the circulating pool of hematopoietic cells and stem cells. These alternative sources of fibroblasts would best be treated by specifically targeting the transition or transdifferentiation process by which cells change into fibroblasts.

Original languageEnglish (US)
Pages (from-to)733-738
Number of pages6
JournalCurrent Opinion in Rheumatology
Volume16
Issue number6
DOIs
StatePublished - Nov 1 2004

Fingerprint

Systemic Scleroderma
Fibrosis
Fibroblasts
Myofibroblasts
Epithelial-Mesenchymal Transition
Amyloidogenic Proteins
Kidney
Blood Proteins
Blood Cells
Epithelial Cells
Pericytes
Transforming Growth Factors
Rheumatic Diseases
Monocytes
Intercellular Signaling Peptides and Proteins
Stem Cells
Epithelium
Cytokines
Bone and Bones
Skin

All Science Journal Classification (ASJC) codes

  • Rheumatology

Cite this

Cellular origins of fibroblasts : Possible implications for organ fibrosis in systemic sclerosis. / Postlethwaite, Arnold; Shigemitsu, Hidenobu; Kanangat, Siva.

In: Current Opinion in Rheumatology, Vol. 16, No. 6, 01.11.2004, p. 733-738.

Research output: Contribution to journalReview article

@article{dad5475d39d345be89f288b418d8b5c2,
title = "Cellular origins of fibroblasts: Possible implications for organ fibrosis in systemic sclerosis",
abstract = "Purpose of review: There is an intense interest in the potential of circulating blood cells and epithelium-related nonfibroblast cells to change into matrix synthesizing fibroblasts and myofibroblasts. These sources of fibroblasts may have importance in systemic sclerosis (scleroderma). Recent findings: Epithelial cells from different sources can transition into fibroblasts and myofibroblasts in response to transforming growth factor β and other growth factors/cytokines. This is called epithelial-mesenchymal transition (EMT). EMT has been repeatedly demonstrated to occur in several models of renal fibrosis including lupus prone mice. Quite unexpectedly, bone morphogenic protein 7 prevents EMT and protects lupus mice and other renal fibrosis models from developing fibrosis in the kidneys. Human peripheral blood mononuclear cells under different conditions of culture give rise to several different types of fibroblast-like cells. In SSc, it has been observed that the sera have low levels of serum amyloid protein. Serum amyloid protein has been found to inhibit the generation of fibrocytes from CD14+ precursors. The implications of these potential sources of fibroblasts and myofibroblasts in systemic sclerosis and related rheumatic diseases are discussed. Summary: Fibroblasts and myofibroblasts in skin and internal organs of patients with systemic sclerosis and related diseases may possibly arise not only from the resident fibroblast population but from epithelial cells, pericytes, monocytes, and other progenitors from the circulating pool of hematopoietic cells and stem cells. These alternative sources of fibroblasts would best be treated by specifically targeting the transition or transdifferentiation process by which cells change into fibroblasts.",
author = "Arnold Postlethwaite and Hidenobu Shigemitsu and Siva Kanangat",
year = "2004",
month = "11",
day = "1",
doi = "10.1097/01.bor.0000139310.77347.9c",
language = "English (US)",
volume = "16",
pages = "733--738",
journal = "Current Opinion in Rheumatology",
issn = "1040-8711",
publisher = "Lippincott Williams and Wilkins",
number = "6",

}

TY - JOUR

T1 - Cellular origins of fibroblasts

T2 - Possible implications for organ fibrosis in systemic sclerosis

AU - Postlethwaite, Arnold

AU - Shigemitsu, Hidenobu

AU - Kanangat, Siva

PY - 2004/11/1

Y1 - 2004/11/1

N2 - Purpose of review: There is an intense interest in the potential of circulating blood cells and epithelium-related nonfibroblast cells to change into matrix synthesizing fibroblasts and myofibroblasts. These sources of fibroblasts may have importance in systemic sclerosis (scleroderma). Recent findings: Epithelial cells from different sources can transition into fibroblasts and myofibroblasts in response to transforming growth factor β and other growth factors/cytokines. This is called epithelial-mesenchymal transition (EMT). EMT has been repeatedly demonstrated to occur in several models of renal fibrosis including lupus prone mice. Quite unexpectedly, bone morphogenic protein 7 prevents EMT and protects lupus mice and other renal fibrosis models from developing fibrosis in the kidneys. Human peripheral blood mononuclear cells under different conditions of culture give rise to several different types of fibroblast-like cells. In SSc, it has been observed that the sera have low levels of serum amyloid protein. Serum amyloid protein has been found to inhibit the generation of fibrocytes from CD14+ precursors. The implications of these potential sources of fibroblasts and myofibroblasts in systemic sclerosis and related rheumatic diseases are discussed. Summary: Fibroblasts and myofibroblasts in skin and internal organs of patients with systemic sclerosis and related diseases may possibly arise not only from the resident fibroblast population but from epithelial cells, pericytes, monocytes, and other progenitors from the circulating pool of hematopoietic cells and stem cells. These alternative sources of fibroblasts would best be treated by specifically targeting the transition or transdifferentiation process by which cells change into fibroblasts.

AB - Purpose of review: There is an intense interest in the potential of circulating blood cells and epithelium-related nonfibroblast cells to change into matrix synthesizing fibroblasts and myofibroblasts. These sources of fibroblasts may have importance in systemic sclerosis (scleroderma). Recent findings: Epithelial cells from different sources can transition into fibroblasts and myofibroblasts in response to transforming growth factor β and other growth factors/cytokines. This is called epithelial-mesenchymal transition (EMT). EMT has been repeatedly demonstrated to occur in several models of renal fibrosis including lupus prone mice. Quite unexpectedly, bone morphogenic protein 7 prevents EMT and protects lupus mice and other renal fibrosis models from developing fibrosis in the kidneys. Human peripheral blood mononuclear cells under different conditions of culture give rise to several different types of fibroblast-like cells. In SSc, it has been observed that the sera have low levels of serum amyloid protein. Serum amyloid protein has been found to inhibit the generation of fibrocytes from CD14+ precursors. The implications of these potential sources of fibroblasts and myofibroblasts in systemic sclerosis and related rheumatic diseases are discussed. Summary: Fibroblasts and myofibroblasts in skin and internal organs of patients with systemic sclerosis and related diseases may possibly arise not only from the resident fibroblast population but from epithelial cells, pericytes, monocytes, and other progenitors from the circulating pool of hematopoietic cells and stem cells. These alternative sources of fibroblasts would best be treated by specifically targeting the transition or transdifferentiation process by which cells change into fibroblasts.

UR - http://www.scopus.com/inward/record.url?scp=7044224913&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=7044224913&partnerID=8YFLogxK

U2 - 10.1097/01.bor.0000139310.77347.9c

DO - 10.1097/01.bor.0000139310.77347.9c

M3 - Review article

VL - 16

SP - 733

EP - 738

JO - Current Opinion in Rheumatology

JF - Current Opinion in Rheumatology

SN - 1040-8711

IS - 6

ER -