ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011
Rab38 targets to lamellar bodies and normalizes their sizes in lung alveolar type II epithelial cells.
Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 32 citations in OpenAlex.
- Overlapping Machinery in Lysosome-Related Organelle Trafficking: A Lesson from Rare Multisystem Disorders.Cells · 2022Review
- Zebrafish Syndromic Albinism Models as Tools for Understanding and Treating Pigment Cell Disease in Humans.Cancers · 2022Review
- Post-correlation on-lamella cryo-CLEM reveals the membrane architecture of lamellar bodies.Communications biology · 2021Article
- Hermansky-Pudlak Syndrome and Lung Disease: Pathogenesis and Therapeutics.Frontiers in pharmacology · 2021Review
- Vascular smooth muscle cell phenotypic transition regulates gap junctions of cardiomyocyte.Heart and vessels · 2020Article
- A novel mutation causes Hermansky-Pudlak syndrome type 4 with pulmonary fibrosis in 2 siblings from China.Medicine · 2019Observational
- The road to lysosome-related organelles: Insights from Hermansky-Pudlak syndrome and other rare diseases.Traffic (Copenhagen, Denmark) · 2019Review
- Review
- Gene-edited MLE-15 Cells as a Model for the Hermansky-Pudlak Syndromes.American journal of respiratory cell and molecular biology · 2018Article
- Exogenous gene transfer of RabRespiratory research · 2017Article
- Pulmonary Fibrosis in Hermansky-Pudlak Syndrome.Annals of the American Thoracic Society · 2016Review
- Impaired Lysosomal Integral Membrane Protein 2-dependent Peroxiredoxin 6 Delivery to Lamellar Bodies Accounts for Altered Alveolar Phospholipid Content in Adaptor Protein-3-deficient pearl Mice.The Journal of biological chemistry · 2016Article
- Rab32 and Rab38 genes in chordate pigmentation: an evolutionary perspective.BMC evolutionary biology · 2016Article
- SNAREs in the maturation and function of LROs.Bioarchitecture · 2016Review
- In vitro functional correction of Hermansky-Pudlak Syndrome type-1 by lentiviral-mediated gene transfer.Molecular genetics and metabolism · 2015Article
- Caenorhabditis elegans HOPS and CCZ-1 mediate trafficking to lysosome-related organelles independently of RAB-7 and SAND-1.Molecular biology of the cell · 2014Article
- Evidence for defective Rab GTPase-dependent cargo traffic in immune disorders.Experimental cell research · 2013Review
- Lysosome-related organelles: unusual compartments become mainstream.Current opinion in cell biology · 2013Review
- Rab38 modulates proteinuria in model of hypertension-associated renal disease.Journal of the American Society of Nephrology : JASN · 2013Article
- Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Rab38 is a rat Hermansky-Pudlak syndrome gene that plays an important role in surfactant homeostasis in alveolar type II (ATII) pneumocytes. We examined Rab38 function in regulating lamellar body (LB) morphology in ATII cells. Quantitative electron microscopy revealed that LBs in ATII cells were ∼77% larger in Rab38-null fawn-hooded hypertension (FHH) than control Sprague-Dawley (SD) rats. Rab38 protein expression was restricted in lung epithelial cells but was not found in primary endothelial cells. In SD ATII cells, Rab38 protein level gradually declined during 5 days in culture. Importantly, endogenous Rab38 was present in LB fractions purified from SD rat lungs, and transiently expressed enhanced green fluorescent protein (EGFP)-tagged Rab38 labeled only the limiting membranes of a subpopulation (∼30%) of LBs in cultured ATII cells. This selective targeting was abolished by point mutations to EGFP-Rab38 and was not shared by Rab7 and Rab4b, which also function in the ATII cells. Using confocal microscopy, we established a method for quantitative evaluation of the enlarged LB phenotype temporally preserved in cultured FHH ATII cells. A direct causal relationship was established when the enlarged LB phenotype was reserved and then rescued by transiently reexpressed EGFP-Rab38 in cultured FHH ATII cells. This rescuing effect was associated with dynamic EGFP-Rab38 targeting to and on LB limiting membranes. We conclude that Rab38 plays an indispensible role in maintaining LB morphology and surfactant homeostasis in ATII pneumocytes.
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Registered trials
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