Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Transcription profiling of mouse lung samples treated with Simvastatin and LPS and corresponded controls

ABSTRACT: This series contain mouse lung samples treated with Simvastatin and LPS and corresponded controls.

ORGANISM(S): Mus musculus

DISEASE(S): LPS-induced acute lung injury

SUBMITTER: Shwu-Fan Ma

PROVIDER: E-GEOD-1871 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Simvastatin attenuates vascular leak and inflammation in murine inflammatory lung injury.

Jacobson Jeffrey R JR Barnard Joseph W JW Grigoryev Dmitry N DN Ma Shwu-Fan SF Tuder Rubin M RM Garcia Joe G N JG

American journal of physiology. Lung cellular and molecular physiology 20050121 6

Therapies to limit the life-threatening vascular leak observed in patients with acute lung injury (ALI) are currently lacking. We explored the effect of simvastatin, a 3-hydroxy-3-methylglutaryl (HMG)-CoA reductase inhibitor that mediates endothelial cell barrier protection in vitro, in a murine inflammatory model of ALI. C57BL/6J mice were treated with simvastatin (5 or 20 mg/kg body wt via intraperitoneal injection) 24 h before and again concomitantly with intratracheally administered LPS (2 m ...[more]

PMID: 15665042

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Project description:Background: Microvascular injury and increased vascular leakage are prominent features of the radiation-induced lung injury (RILI) which follows cancer–associated thoracic irradiation. The mechanisms of RILI are incompletely understood and therapeutic strategies to limit RILI are currently unavailable. We established a murine model of radiation pneumonitis in order to assess mechanism-based therapies for RILI-induced inflammation and vascular barrier dysfunction. Based on prior studies, we investigated the therapeutic potential of simvastatin as a vascular barrier protective agent in RILI. Methods: C57BL6/J mice receiving single dose exposure to 18, 20, 22, or 25 Gy, (n=10/group) were temporally assessed (4-12 weeks) for cellular and biochemical indices of injury present in both bronchoalveolar lavage (BAL) and lung tissues (cytokines, tyrosine nitrosylated proteins, leukocytes, extravasation of Evans blue dye or EBD, BAL albumin, histology). In specific experiments, irradiated mice (25Gy) received simvastatin (10 mg/kg) via intraperitoneal injection three times a week (pre and post irradiation) for 2- 6 weeks post irradiation. Results. Acute RILI evolved in a dose- and time-dependent fashion. Mice irradiated with 25Gy exhibited modest increases in BAL leukocytes but significant increases in BAL IL-6 (p=0.03) and TNF-a (p=0.01) at 4 weeks compared to controls. Increases in BAL nitrotyrosine content peaked at 6 weeks (p=0.03) and was accompanied by marked nitrotyrosine immunostaining in lung tissues. Indices of increase lung vascular permeability such as EBD extravasation, BAL protein and BAL albumin significantly increased over time beginning at 6 weeks (p>0.002 all) with histological evidence of severe edema formation and airway inflammation. Simvastatin- treated irradiated mice were noted to exhibit marked attenuation of vascular leak with significantly decreased BAL protein (p=0.01) and inflammatory cell infiltration (50% reduction). Conclusion: Simvastatin is a potentially important therapeutic strategy to limit RILI and may influence radiation associated morbidity and mortality. We used microarrays to detail the global programme of gene expression induced by radiation in Wild type and the protection of SIMVA

Dataset Information

Transcription profiling of mouse lung samples treated with Simvastatin and LPS and corresponded controls

Publications

Simvastatin attenuates vascular leak and inflammation in murine inflammatory lung injury.

Similar Datasets

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