Marked disruption and aberrant regulation of elastic fibres in early striae gravidarum

F. Wang, K. Calderone, N. R. Smith, T. T. Do, Y. R. Helfrich, T. R B Johnson, Sewon Kang, J. J. Voorhees, G. J. Fisher

Research output: Contribution to journalArticle

Abstract

Background Striae gravidarum (SG), or 'stretch marks' of pregnancy, begin as erythematous streaks, and mature over months to years to become permanent scar-like bands that may be hypopigmented, atrophic and lax. Objectives To investigate early molecular alterations that may promote laxity of mature SG, we investigated the dermal elastic fibre network, which provides human skin with elastic properties. Methods We obtained skin samples of newly developed, erythematous abdominal SG in healthy pregnant women. The elastic fibre network was examined by Verhoeff elastic staining and immunofluorescence staining of skin sections. Gene expression was measured by real-time polymerase chain reaction. Results The normal elastic fibre network appeared markedly disrupted in SG, compared with perilesional abdominal skin or control (normal-appearing hip skin). This disruption was accompanied by the emergence of short, disorganized, thin, thread-like 'fibrils', which were observed prominently in the mid-to-deep dermis. These fibrils were rich in tropoelastin (the main component of normal elastic fibres), and persisted into the postpartum period without forming normal-appearing elastic fibres. The emergence of these fibrils was accompanied by increased gene expression of tropoelastin and fibrillin-1, but not other elastic fibre components, including fibrillin-2 and fibulin-1, -2 or -5. Conclusions In early SG, the elastic fibre network appears markedly disrupted, and newly synthesized tropoelastin-rich fibrils emerge, likely as a result of uncoordinated synthesis of elastic fibre components. Because they are thin and disorganized, tropoelastin-rich fibrils likely do not function as normal elastic fibres do. These observations provide the foundations for elucidating pathogenic mechanisms by which laxity may develop in SG.

Original languageEnglish (US)
Pages (from-to)1420-1430
Number of pages11
JournalBritish Journal of Dermatology
Volume173
Issue number6
DOIs
StatePublished - Dec 1 2015
Externally publishedYes

Fingerprint

Elastic Tissue
Tropoelastin
Skin
Striae Distensae
Staining and Labeling
Gene Expression
Dermis
Postpartum Period
Cicatrix
Fluorescent Antibody Technique
Hip
Real-Time Polymerase Chain Reaction
Pregnant Women
Pregnancy

ASJC Scopus subject areas

  • Medicine(all)
  • Dermatology

Cite this

Wang, F., Calderone, K., Smith, N. R., Do, T. T., Helfrich, Y. R., Johnson, T. R. B., ... Fisher, G. J. (2015). Marked disruption and aberrant regulation of elastic fibres in early striae gravidarum. British Journal of Dermatology, 173(6), 1420-1430. https://doi.org/10.1111/bjd.14027

Marked disruption and aberrant regulation of elastic fibres in early striae gravidarum. / Wang, F.; Calderone, K.; Smith, N. R.; Do, T. T.; Helfrich, Y. R.; Johnson, T. R B; Kang, Sewon; Voorhees, J. J.; Fisher, G. J.

In: British Journal of Dermatology, Vol. 173, No. 6, 01.12.2015, p. 1420-1430.

Research output: Contribution to journalArticle

Wang, F, Calderone, K, Smith, NR, Do, TT, Helfrich, YR, Johnson, TRB, Kang, S, Voorhees, JJ & Fisher, GJ 2015, 'Marked disruption and aberrant regulation of elastic fibres in early striae gravidarum', British Journal of Dermatology, vol. 173, no. 6, pp. 1420-1430. https://doi.org/10.1111/bjd.14027
Wang F, Calderone K, Smith NR, Do TT, Helfrich YR, Johnson TRB et al. Marked disruption and aberrant regulation of elastic fibres in early striae gravidarum. British Journal of Dermatology. 2015 Dec 1;173(6):1420-1430. https://doi.org/10.1111/bjd.14027
Wang, F. ; Calderone, K. ; Smith, N. R. ; Do, T. T. ; Helfrich, Y. R. ; Johnson, T. R B ; Kang, Sewon ; Voorhees, J. J. ; Fisher, G. J. / Marked disruption and aberrant regulation of elastic fibres in early striae gravidarum. In: British Journal of Dermatology. 2015 ; Vol. 173, No. 6. pp. 1420-1430.
@article{392568710b5b4675b806decde2032899,
title = "Marked disruption and aberrant regulation of elastic fibres in early striae gravidarum",
abstract = "Background Striae gravidarum (SG), or 'stretch marks' of pregnancy, begin as erythematous streaks, and mature over months to years to become permanent scar-like bands that may be hypopigmented, atrophic and lax. Objectives To investigate early molecular alterations that may promote laxity of mature SG, we investigated the dermal elastic fibre network, which provides human skin with elastic properties. Methods We obtained skin samples of newly developed, erythematous abdominal SG in healthy pregnant women. The elastic fibre network was examined by Verhoeff elastic staining and immunofluorescence staining of skin sections. Gene expression was measured by real-time polymerase chain reaction. Results The normal elastic fibre network appeared markedly disrupted in SG, compared with perilesional abdominal skin or control (normal-appearing hip skin). This disruption was accompanied by the emergence of short, disorganized, thin, thread-like 'fibrils', which were observed prominently in the mid-to-deep dermis. These fibrils were rich in tropoelastin (the main component of normal elastic fibres), and persisted into the postpartum period without forming normal-appearing elastic fibres. The emergence of these fibrils was accompanied by increased gene expression of tropoelastin and fibrillin-1, but not other elastic fibre components, including fibrillin-2 and fibulin-1, -2 or -5. Conclusions In early SG, the elastic fibre network appears markedly disrupted, and newly synthesized tropoelastin-rich fibrils emerge, likely as a result of uncoordinated synthesis of elastic fibre components. Because they are thin and disorganized, tropoelastin-rich fibrils likely do not function as normal elastic fibres do. These observations provide the foundations for elucidating pathogenic mechanisms by which laxity may develop in SG.",
author = "F. Wang and K. Calderone and Smith, {N. R.} and Do, {T. T.} and Helfrich, {Y. R.} and Johnson, {T. R B} and Sewon Kang and Voorhees, {J. J.} and Fisher, {G. J.}",
year = "2015",
month = "12",
day = "1",
doi = "10.1111/bjd.14027",
language = "English (US)",
volume = "173",
pages = "1420--1430",
journal = "British Journal of Dermatology",
issn = "0007-0963",
publisher = "Wiley-Blackwell",
number = "6",

}

TY - JOUR

T1 - Marked disruption and aberrant regulation of elastic fibres in early striae gravidarum

AU - Wang, F.

AU - Calderone, K.

AU - Smith, N. R.

AU - Do, T. T.

AU - Helfrich, Y. R.

AU - Johnson, T. R B

AU - Kang, Sewon

AU - Voorhees, J. J.

AU - Fisher, G. J.

PY - 2015/12/1

Y1 - 2015/12/1

N2 - Background Striae gravidarum (SG), or 'stretch marks' of pregnancy, begin as erythematous streaks, and mature over months to years to become permanent scar-like bands that may be hypopigmented, atrophic and lax. Objectives To investigate early molecular alterations that may promote laxity of mature SG, we investigated the dermal elastic fibre network, which provides human skin with elastic properties. Methods We obtained skin samples of newly developed, erythematous abdominal SG in healthy pregnant women. The elastic fibre network was examined by Verhoeff elastic staining and immunofluorescence staining of skin sections. Gene expression was measured by real-time polymerase chain reaction. Results The normal elastic fibre network appeared markedly disrupted in SG, compared with perilesional abdominal skin or control (normal-appearing hip skin). This disruption was accompanied by the emergence of short, disorganized, thin, thread-like 'fibrils', which were observed prominently in the mid-to-deep dermis. These fibrils were rich in tropoelastin (the main component of normal elastic fibres), and persisted into the postpartum period without forming normal-appearing elastic fibres. The emergence of these fibrils was accompanied by increased gene expression of tropoelastin and fibrillin-1, but not other elastic fibre components, including fibrillin-2 and fibulin-1, -2 or -5. Conclusions In early SG, the elastic fibre network appears markedly disrupted, and newly synthesized tropoelastin-rich fibrils emerge, likely as a result of uncoordinated synthesis of elastic fibre components. Because they are thin and disorganized, tropoelastin-rich fibrils likely do not function as normal elastic fibres do. These observations provide the foundations for elucidating pathogenic mechanisms by which laxity may develop in SG.

AB - Background Striae gravidarum (SG), or 'stretch marks' of pregnancy, begin as erythematous streaks, and mature over months to years to become permanent scar-like bands that may be hypopigmented, atrophic and lax. Objectives To investigate early molecular alterations that may promote laxity of mature SG, we investigated the dermal elastic fibre network, which provides human skin with elastic properties. Methods We obtained skin samples of newly developed, erythematous abdominal SG in healthy pregnant women. The elastic fibre network was examined by Verhoeff elastic staining and immunofluorescence staining of skin sections. Gene expression was measured by real-time polymerase chain reaction. Results The normal elastic fibre network appeared markedly disrupted in SG, compared with perilesional abdominal skin or control (normal-appearing hip skin). This disruption was accompanied by the emergence of short, disorganized, thin, thread-like 'fibrils', which were observed prominently in the mid-to-deep dermis. These fibrils were rich in tropoelastin (the main component of normal elastic fibres), and persisted into the postpartum period without forming normal-appearing elastic fibres. The emergence of these fibrils was accompanied by increased gene expression of tropoelastin and fibrillin-1, but not other elastic fibre components, including fibrillin-2 and fibulin-1, -2 or -5. Conclusions In early SG, the elastic fibre network appears markedly disrupted, and newly synthesized tropoelastin-rich fibrils emerge, likely as a result of uncoordinated synthesis of elastic fibre components. Because they are thin and disorganized, tropoelastin-rich fibrils likely do not function as normal elastic fibres do. These observations provide the foundations for elucidating pathogenic mechanisms by which laxity may develop in SG.

UR - http://www.scopus.com/inward/record.url?scp=84983122448&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84983122448&partnerID=8YFLogxK

U2 - 10.1111/bjd.14027

DO - 10.1111/bjd.14027

M3 - Article

C2 - 26179468

AN - SCOPUS:84983122448

VL - 173

SP - 1420

EP - 1430

JO - British Journal of Dermatology

JF - British Journal of Dermatology

SN - 0007-0963

IS - 6

ER -