The Pulmonary Lipofibroblast (Lipid Interstitial Cell) and Its Contributions to Alveolar Development

McGowan, Stephen E.; Torday, John S.

doi:10.1146/annurev.physiol.59.1.43

Cited by 199 publications

(192 citation statements)

References 63 publications

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“…The situation in the developing lung is unusual in that a large amount of surfactant has to be produced within a short period of time. Lipid-laden lung fibroblasts (lipofibroblasts;McGowan & Torday 1997) are transiently observed during the perinatal period in the developing lung (Maksvytis et al 1981, Tordet et al 1981 where they are involved in lipid storage for surfactant production by PTII cells (Nunez & Torday 1995. In fact, triglyceride uptake by fibroblasts increases nine fold in the fetal rat lung between GDs 17 and 21.…”

Section: Discussionmentioning

confidence: 99%

Apolipoprotein A-I, A-II, C-II, and H expression in the developing lung and sex difference in surfactant lipids

Provost¹,

Boucher²,

Tremblay³

2008

Journal of Endocrinology

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A sex difference in surfactant lipids is associated with a higher incidence of respiratory distress syndrome for males in cases of preterm birth. In animal models, the sex difference in surfactant lipids was shown to be androgen receptordependent. This report examines expression of apolipoprotein (apo)A-I, apoA-II, apoC-II, apoE, apoH, and lipoprotein lipase (LPL) by quantitative real-time PCR in pools of male and female fetal lung tissues from various mouse litters from gestation day (GD) 15 . 5 to 18 . 5, and in various adult tissues.Although the expression profiles of ApoA-I, ApoA-II, ApoC-II, and ApoH are complex, these genes are co-regulated and they all present a sex difference (PZ0 . 0896, 0 . 0896, 0 . 0195, and 0 . 0607 respectively) with higher expression for females for several litters. Pulmonary expression of apoA-I, apoA-II, and apoH were specific to the developing lung. ApoE and LPL mRNAs showed a significant increase from GD 17 . 5 to 18 . 5. An increase in apoA-I-, apoA-II-, apoC-II-, and apoHmRNA accumulation was observed from GD 16 . 5 to 17 . 5 in correlation with the emergence of mature type II pneumonocytes. These four apolipoprotein genes are co-regulated with type 2 and 5 17b-hydroxysteroid dehydrogenases, which are respectively involved in inactivation and synthesis of androgens. Finally, apoC-II was detected by immunohistochemistry in epithelial cells of the distal epithelium. Positive signals looking like secretory granules were located near the basal membrane. Our results are compatible with a role for apolipoproteins in lipid metabolism and transport in the developing lung in association with the sex difference in surfactant lipid synthesis.

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Section: Discussionmentioning

confidence: 99%

Apolipoprotein A-I, A-II, C-II, and H expression in the developing lung and sex difference in surfactant lipids

Provost¹,

Boucher²,

Tremblay³

2008

Journal of Endocrinology

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“…Although much less is known about the support roles that mesenchymal cells play in the adult lung, recent work emphasizes potential roles for pericytes as vascular support cells (39,40), whereas parenchymal lipofibroblasts are believed to serve as alveolar epithelial support cells (43)(44)(45). Although methods to identify and study these mesenchymal subpopulations in mouse models are rapidly emerging, more definitive markers of these (and other) mesenchymal cell subpopulations are needed to understand their localization in human lungs and their potential contributions to lung diseases.…”

Section: Matrix and Mesenchyme In Development And Homeostasismentioning

confidence: 99%

Matrix, Mesenchyme, and Mechanotransduction

Tschumperlin

2015

Annals ATS

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The extracellular matrix (ECM) of the lung serves as both a scaffold for resident cells and a mechanical support for respiratory function. The ECM is deposited during development and undergoes continuous turnover and maintenance during organ growth and homeostasis. Cells of the mesenchyme, including the tissue resident fibroblast, take a leading role in depositing and organizing the matrix and do so in an anatomically distinct fashion, with differing composition, organization, and mechanical properties within the airways, vessels, and alveoli of the lung. Recent technological advancements have allowed the lung's ECM biochemical composition and mechanical properties to be studied with improved resolution, thereby identifying novel disease-related changes in ECM characteristics. In parallel, efforts to study cells seeded on normal and disease-derived matrices have illustrated the powerful role the ECM can play in altering key functions of lung resident cells. The mechanical properties of the matrix have been identified as an important modifier of cell-matrix adhesions, with matrices of pathologic stiffness promoting profibrotic signaling and cell function. Ongoing work is identifying both mechanically activated pathways in mesenchymal cells and diseaserelated ECM molecules that biochemically regulate cell function. Uncovering the control systems by which cells respond to and regulate the matrix, and the failures in these systems that underlie aberrant repair, remains a major challenge. Progress in this area will be an essential element in efforts to engineer functional lung tissue for regenerative approaches and will be key to identifying new therapeutic strategies for lung diseases characterized by disturbed matrix architecture.

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“…In those mice, alveolarization is delayed, but they finally form normal lungs (Sonja Mund and J.C.S., unpublished results). The alterations in cellular number and phenotype seen in older mutant lungs could in principle be a secondary consequence of the ECM alterations present at P1 (e.g., McGowan and Torday, 1997;Neptune et al, 2003;Thannickal et al, 2003); or could reflect an independent requirement for ephrinB2 function.…”

Section: Ecm Differences Precede Cell Number Changes In P1 Mutant Lungmentioning

confidence: 99%

Role for ephrinB2 in postnatal lung alveolar development and elastic matrix integrity

Wilkinson

Schittny

Reinhardt

et al. 2008

Developmental Dynamics

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Alveoli are formed in the lung by the insertion of secondary tissue folds, termed septa, which are subsequently remodeled to form the mature alveolar wall. Secondary septation requires interplay between three cell types: endothelial cells forming capillaries, contractile interstitial myofibroblasts, and epithelial cells. Here, we report that postnatal lung alveolization critically requires ephrinB2, a ligand for Eph receptor tyrosine kinases expressed by the microvasculature. Mice homozygous for the hypomorphic knockin allele ephrinB2 ⌬V/⌬V , encoding mutant ephrinB2 with a disrupted C-terminal PDZ interaction motif, show severe postnatal lung defects including an almost complete absence of lung alveoli and abnormal and disorganized elastic matrix. Lung alveolar formation is not sensitive to loss of ephrinB2 cytoplasmic tyrosine phosphorylation sites. Postnatal day 1 mutant lungs show extracellular matrix alterations without differences in proportions of major distal cell populations. We conclude that lung alveolar formation relies on endothelial ephrinB2 function. Developmental Dynamics 237:2220 -2234, 2008.

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The Pulmonary Lipofibroblast (Lipid Interstitial Cell) and Its Contributions to Alveolar Development

Cited by 199 publications

References 63 publications

Apolipoprotein A-I, A-II, C-II, and H expression in the developing lung and sex difference in surfactant lipids

Apolipoprotein A-I, A-II, C-II, and H expression in the developing lung and sex difference in surfactant lipids

Matrix, Mesenchyme, and Mechanotransduction

Role for ephrinB2 in postnatal lung alveolar development and elastic matrix integrity

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