Improved Movat Pentachrome Stain

Garvey, Winsome; Fathi, Arleen; Bigelow, Francine; Carpenter, Blair; Jimenez, Carmencita

doi:10.3109/10520298609110708

Cited by 47 publications

(34 citation statements)

References 1 publication

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“…Proliferation Index is calculated as the ratio of BrdU-positive VSMCs to unstained medial nuclei in each section. 6 Proteoglycan deposition was quantified using Movat's pentachrome staining 9 and computerized quantification of positive (blue) regions ( Figure 2). For all statistical analyses, genotype and treatment groups were independent variables and thus analyzed using a 2-factor ANOVA, with post hoc pairwise comparisons made with the Student-Newman-Keuls test.…”

Section: Morphometry and Immunohistochemistrymentioning

confidence: 99%

Estrogen Receptor-α Mediates the Protective Effects of Estrogen Against Vascular Injury

Pare

Krust

Karas

et al. 2002

Circulation Research

347

250

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Abstract-Blood vessel cells express the 2 known estrogen receptors, ␣ and ␤ (ER␣, ER␤), which are thought to mediate estrogen inhibition of vascular injury and atherosclerosis, but the relative role of ER␣ and ER␤ in these events is controversial. Key Words: estrogen Ⅲ hormones Ⅲ vascular injury Ⅲ receptors Ⅲ animal models T he cardiovascular effects of steroid hormones are an area of intense interest at present. Estrogen has known systemic effects on circulating factors and has more recently been established to have direct effects on the blood vessel wall. Estrogen causes both rapid vascular dilatation and longer-term effects on gene expression in vascular cells (reviewed in Mendelsohn and Karas 1 ). At physiologically relevant concentrations of estrogen, studies support that estrogen receptors (ERs) ␣ and ␤ mediate both the rapid and the long-term cardiovascular effects of estrogen. ER␣ and ER␤ are expressed in both vascular endothelial and smooth muscle cells, but their physiological roles in the vasculature are incompletely understood.Using wild-type and estrogen receptor knockout mice, we have previously studied the role of ER␣ and ER␤ in mediating the vascular protective effects of estrogen in a mouse carotid artery injury model. 2,3,5,6 Studies of mice harboring single gene deletions of either ER␣ or ER␤ showed that treatment of ovariectomized female mice with nanomolar concentrations of 17␤-estradiol (E 2 ) inhibits the response to vascular injury to equivalent levels in wild-type mice, ER␣KO Chapel Hill (ER␣KO CH ) and ER␤KO CH . 2,5 These findings suggested that ER␣ and ER␤ are able to complement one another such that each receptor alone is sufficient to mediate the vascular protective effects of estrogen, or that the vascular protective effects of estrogen are mediated by an ER␣/ER␤-independent pathway. To distinguish between these 2 hypotheses, studies of vascular injury in ER␣,␤KO CH (double) estrogen receptor knockout mice were performed. 6 However, the effect of estrogen on vascular injury in these mice was complex. Although E 2 no longer inhibited the increases in medial carotid area after injury in the ER␣,␤KO CH mice, E 2 still significantly inhibited vascular smooth muscle cell (VSMC) proliferation after injury. In addition, E 2 also caused a significant increase in uterine weight in the ER␣,␤KO CH mice. 6 These data showed that the role of estrogen receptors could diverge for specific components of the vascular injury response in the ER␣,␤KO CH mice. However, the results left unresolved what is responsible for estrogen inhibition of VSMC proliferation and the increase in uterine weight in the ER␣,␤KO CH mice. These could be due to an unidentified third estrogen receptor or to residual function of protein from an ER␣ splice variant known to be expressed in the parental ER␣KO CH mice. 7 To resolve the question as to how estrogen Original

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Section: Morphometry and Immunohistochemistrymentioning

confidence: 99%

Estrogen Receptor-α Mediates the Protective Effects of Estrogen Against Vascular Injury

Pare

Krust

Karas

et al. 2002

Circulation Research

347

250

View full text Add to dashboard Cite

show abstract

“…Kidneys were fixed in 2% paraformaldehyde overnight at 4°C, decalcified for 2 wk at 4°C using 19% EDTA solution, and embedded in optimal cutting temperature for cryosectioning. Representative sections were stained with Movat's Pentachrome stain (39). To quantify kidney grafts, analytical software (Adobe Photoshop CS6) was used to measure pixel area of engrafted bone specimens.…”

Section: Transplantation Of Skeletal Progenitor Subsets and Analysis mentioning

confidence: 99%

Identification and characterization of an injury-induced skeletal progenitor

Marecic

Tevlin

McArdle

et al. 2015

Proc. Natl. Acad. Sci. U.S.A.

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The postnatal skeleton undergoes growth, remodeling, and repair. We hypothesized that skeletal progenitor cells active during these disparate phases are genetically and phenotypically distinct. We identified a highly potent regenerative cell type that we term the fracture-induced bone, cartilage, stromal progenitor (f-BCSP) in the fracture callus of adult mice. The f-BCSP possesses significantly enhanced skeletogenic potential compared with BCSPs harvested from uninjured bone. It also recapitulates many gene expression patterns involved in perinatal skeletogenesis. Our results indicate that the skeletal progenitor population is functionally stratified, containing distinct subsets responsible for growth, regeneration, and repair. Furthermore, our findings suggest that injury-induced changes to the skeletal stem and progenitor microenvironments could activate these cells and enhance their regenerative potential.osteogenesis | skeletal stem/progenitor cell | fracture healing | regeneration | injury activation

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“…Sections (5 mm) were placed onto polysine slides for immunohistochemistry. Sections were stained with hematoxalin and eosin, Gomori's trichrome stain, or pentachrome for detection of collagen and extracellular matrix deposition (12).…”

Section: Lung Histology and Immunohistochemistrymentioning

confidence: 99%

Genomic Profile of Matrix and Vasculature Remodeling in TGF-α–Induced Pulmonary Fibrosis

Hardie

Korfhagen

Sartor

et al. 2007

Am J Respir Cell Mol Biol

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Expression of transforming growth factor a (TGF-a) in the respiratory epithelium of transgenic mice caused pulmonary fibrosis, cachexia, pulmonary hypertension, and altered lung function. To identify genes and molecular pathways mediating lung remodeling, mRNA microarray analysis was performed at multiple times after TGF-a expression and revealed changes consistent with a role for TGF-a in the regulation of extracellular matrix and vasculogenesis. Transcripts for extracellular matrix proteins were augmented along with transcripts for genes previously identified to have roles in pulmonary fibrosis, including tenascin C, osteopontin, and serine (or cysteine) peptidase inhibitor, clade F, member 1. Transcripts regulating vascular processes including endothelin receptor type B, endothelial-specific receptor tyrosine kinase, and caveolin, caveolae protein 1 were decreased. When TGF-a expression was no longer induced, lung remodeling partially reversed and lung function and pulmonary hypertension normalized. Transcripts increased during resolution included midkine, matrix metalloproteinase 2, and hemolytic complement. Hierarchical clustering revealed that genes regulated by TGF-a were similar to those altered in the lungs of patients with idiopathic pulmonary fibrosis. These studies support a role for epithelial cell-derived TGF-a in the regulation of processes that alter the airway and vascular architecture and function.

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Improved Movat Pentachrome Stain

Cited by 47 publications

References 1 publication

Estrogen Receptor-α Mediates the Protective Effects of Estrogen Against Vascular Injury

Estrogen Receptor-α Mediates the Protective Effects of Estrogen Against Vascular Injury

Identification and characterization of an injury-induced skeletal progenitor

Genomic Profile of Matrix and Vasculature Remodeling in TGF-α–Induced Pulmonary Fibrosis

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