Correction to: FoxD1-driven CCN2 deletion causes axial skeletal deformities, pulmonary hypoplasia, and neonatal asphyctic death (vol 291, pg 5410, 2020) (2024)

Falke, L. L., He, N., Chuva de Sousa Lopes, S. M., Broekhuizen, R., Lyons, K., Nguyen, T. Q., & Goldschmeding, R. (2020). Correction to: FoxD1-driven CCN2 deletion causes axial skeletal deformities, pulmonary hypoplasia, and neonatal asphyctic death (vol 291, pg 5410, 2020). Journal of Cell Communication and Signaling, 14(1), 47-52. https://doi.org/10.1007/s12079-020-00559-2

Falke, Lucas L ; He, Nannan ; Chuva de Sousa Lopes, Susana M et al. / Correction to: FoxD1-driven CCN2 deletion causes axial skeletal deformities, pulmonary hypoplasia, and neonatal asphyctic death (vol 291, pg 5410, 2020). In: Journal of Cell Communication and Signaling. 2020 ; Vol. 14, No. 1. pp. 47-52.

@article{cb51ea000c564b91a9665d9d557ba7d5,

title = "Correction to: FoxD1-driven CCN2 deletion causes axial skeletal deformities, pulmonary hypoplasia, and neonatal asphyctic death (vol 291, pg 5410, 2020)",

abstract = "Pulmonary fibrosis is a severely disabling disease often leading to death. CCN2 (Cellular Communication Network factor 2, also known as CTGF) is a known mediator of fibrosis and clinical trials studying anti-CCN2 efficacy in pulmonary fibrosis are currently underway. Fork head box D1 (FoxD1) transcription factor is transiently expressed in several mesenchymal cell types, including those of fetal lungs. Differentiation of FoxD1-progenitor derived pericytes into myofibroblasts involves CCN2 expression and contributes importantly to maladaptive tissue remodeling in for example kidney and lung fibrosis models. To generate a model for studying the contribution of CCN2 expression in FoxD1-progenitor derived cells to development of fibrotic tissue remodeling, we set out to establish a FoxD1Cre - CCN2flox/flox mouse colony. However, all double-transgenic mice died soon after birth due to asphyxia. Histopathological examination revealed a reduction in alveolar space and lung weight, and subtle axial (thoracic and cervical) skeletal deformities. Together with the previously reported association of a FoxD1 containing locus with human adolescent idiopathic scoliosis, our data suggest that the fatal pulmonary hypoplasia resulting from selective deletion of CCN2 from FoxD1-progenitor derived mesenchymal cells developed secondary to impaired breathing movements due to aberrant axial skeletogenesis.",

keywords = "CCN2, CTGF, FoxD1, Hypoplasia, Lung, Skeletogenesis",

author = "Falke, {Lucas L} and Nannan He and {Chuva de Sousa Lopes}, {Susana M} and Roel Broekhuizen and Karen Lyons and Nguyen, {Tri Q} and Roel Goldschmeding",

note = "Publisher Copyright: {\textcopyright} 2020, The International CCN Society. Copyright: Copyright 2020 Elsevier B.V., All rights reserved.",

year = "2020",

month = mar,

day = "1",

doi = "10.1007/s12079-020-00559-2",

language = "English",

volume = "14",

pages = "47--52",

journal = "Journal of Cell Communication and Signaling",

issn = "1873-9601",

publisher = "Springer Netherlands",

number = "1",

}

Falke, LL, He, N, Chuva de Sousa Lopes, SM, Broekhuizen, R, Lyons, K, Nguyen, TQ & Goldschmeding, R 2020, 'Correction to: FoxD1-driven CCN2 deletion causes axial skeletal deformities, pulmonary hypoplasia, and neonatal asphyctic death (vol 291, pg 5410, 2020)', Journal of Cell Communication and Signaling, vol. 14, no. 1, pp. 47-52. https://doi.org/10.1007/s12079-020-00559-2

Correction to: FoxD1-driven CCN2 deletion causes axial skeletal deformities, pulmonary hypoplasia, and neonatal asphyctic death (vol 291, pg 5410, 2020). / Falke, Lucas L; He, Nannan; Chuva de Sousa Lopes, Susana M et al.
In: Journal of Cell Communication and Signaling, Vol. 14, No. 1, 01.03.2020, p. 47-52.

Research output: Contribution to journal › Article › Academic › peer-review

TY - JOUR

T1 - Correction to: FoxD1-driven CCN2 deletion causes axial skeletal deformities, pulmonary hypoplasia, and neonatal asphyctic death (vol 291, pg 5410, 2020)

AU - Falke, Lucas L

AU - He, Nannan

AU - Chuva de Sousa Lopes, Susana M

AU - Broekhuizen, Roel

AU - Lyons, Karen

AU - Nguyen, Tri Q

AU - Goldschmeding, Roel

N1 - Publisher Copyright:© 2020, The International CCN Society.Copyright:Copyright 2020 Elsevier B.V., All rights reserved.

PY - 2020/3/1

Y1 - 2020/3/1

N2 - Pulmonary fibrosis is a severely disabling disease often leading to death. CCN2 (Cellular Communication Network factor 2, also known as CTGF) is a known mediator of fibrosis and clinical trials studying anti-CCN2 efficacy in pulmonary fibrosis are currently underway. Fork head box D1 (FoxD1) transcription factor is transiently expressed in several mesenchymal cell types, including those of fetal lungs. Differentiation of FoxD1-progenitor derived pericytes into myofibroblasts involves CCN2 expression and contributes importantly to maladaptive tissue remodeling in for example kidney and lung fibrosis models. To generate a model for studying the contribution of CCN2 expression in FoxD1-progenitor derived cells to development of fibrotic tissue remodeling, we set out to establish a FoxD1Cre - CCN2flox/flox mouse colony. However, all double-transgenic mice died soon after birth due to asphyxia. Histopathological examination revealed a reduction in alveolar space and lung weight, and subtle axial (thoracic and cervical) skeletal deformities. Together with the previously reported association of a FoxD1 containing locus with human adolescent idiopathic scoliosis, our data suggest that the fatal pulmonary hypoplasia resulting from selective deletion of CCN2 from FoxD1-progenitor derived mesenchymal cells developed secondary to impaired breathing movements due to aberrant axial skeletogenesis.

AB - Pulmonary fibrosis is a severely disabling disease often leading to death. CCN2 (Cellular Communication Network factor 2, also known as CTGF) is a known mediator of fibrosis and clinical trials studying anti-CCN2 efficacy in pulmonary fibrosis are currently underway. Fork head box D1 (FoxD1) transcription factor is transiently expressed in several mesenchymal cell types, including those of fetal lungs. Differentiation of FoxD1-progenitor derived pericytes into myofibroblasts involves CCN2 expression and contributes importantly to maladaptive tissue remodeling in for example kidney and lung fibrosis models. To generate a model for studying the contribution of CCN2 expression in FoxD1-progenitor derived cells to development of fibrotic tissue remodeling, we set out to establish a FoxD1Cre - CCN2flox/flox mouse colony. However, all double-transgenic mice died soon after birth due to asphyxia. Histopathological examination revealed a reduction in alveolar space and lung weight, and subtle axial (thoracic and cervical) skeletal deformities. Together with the previously reported association of a FoxD1 containing locus with human adolescent idiopathic scoliosis, our data suggest that the fatal pulmonary hypoplasia resulting from selective deletion of CCN2 from FoxD1-progenitor derived mesenchymal cells developed secondary to impaired breathing movements due to aberrant axial skeletogenesis.

KW - CCN2

KW - CTGF

KW - FoxD1

KW - Hypoplasia

KW - Lung

KW - Skeletogenesis

UR - http://www.scopus.com/inward/record.url?scp=85083680046&partnerID=8YFLogxK

U2 - 10.1007/s12079-020-00559-2

DO - 10.1007/s12079-020-00559-2

M3 - Article

C2 - 32291573

SN - 1873-9601

VL - 14

SP - 47

EP - 52

JO - Journal of Cell Communication and Signaling

JF - Journal of Cell Communication and Signaling

IS - 1

ER -

Falke LL, He N, Chuva de Sousa Lopes SM, Broekhuizen R, Lyons K, Nguyen TQ et al. Correction to: FoxD1-driven CCN2 deletion causes axial skeletal deformities, pulmonary hypoplasia, and neonatal asphyctic death (vol 291, pg 5410, 2020). Journal of Cell Communication and Signaling. 2020 Mar 1;14(1):47-52. doi: 10.1007/s12079-020-00559-2