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  • 1
    Online Resource
    Online Resource
    Conditional Ablation of Macrophages Halts Progression of Crescentic Glomerulonephritis
    Elsevier BV ; 2005
    In:  The American Journal of Pathology Vol. 167, No. 5 ( 2005-11), p. 1207-1219
    Details
    In: The American Journal of Pathology, Elsevier BV, Vol. 167, No. 5 ( 2005-11), p. 1207-1219
    Type of Medium: Online Resource
    ISSN: 0002-9440
    URL: Article
    DOI: 10.1016/S0002-9440(10)61209-6
    RVK:
    XA 10000
    RVK:
    XA 19800
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2005
    detail.hit.zdb_id: 1480207-7
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  • 2
    Online Resource
    Online Resource
    The bHLH transcription factor Tcf21 is required for lineage-specific EMT of cardiac fibroblast progenitors
    The Company of Biologists ; 2012
    In:  Development Vol. 139, No. 12 ( 2012-06-15), p. 2139-2149
    Details
    In: Development, The Company of Biologists, Vol. 139, No. 12 ( 2012-06-15), p. 2139-2149
    Abstract: The basic helix-loop-helix (bHLH) family of transcription factors orchestrates cell-fate specification, commitment and differentiation in multiple cell lineages during development. Here, we describe the role of a bHLH transcription factor, Tcf21 (epicardin/Pod1/capsulin), in specification of the cardiac fibroblast lineage. In the developing heart, the epicardium constitutes the primary source of progenitor cells that form two cell lineages: coronary vascular smooth muscle cells (cVSMCs) and cardiac fibroblasts. Currently, there is a debate regarding whether the specification of these lineages occurs early in the formation of the epicardium or later after the cells have entered the myocardium. Lineage tracing using a tamoxifen-inducible Cre expressed from the Tcf21 locus demonstrated that the majority of Tcf21-expressing epicardial cells are committed to the cardiac fibroblast lineage prior to initiation of epicardial epithelial-to-mesenchymal transition (EMT). Furthermore, Tcf21 null hearts fail to form cardiac fibroblasts, and lineage tracing of the null cells showed their inability to undergo EMT. This is the first report of a transcription factor essential for the development of cardiac fibroblasts. We demonstrate a unique role for Tcf21 in multipotent epicardial progenitors, prior to the process of EMT that is essential for cardiac fibroblast development.
    Type of Medium: Online Resource
    ISSN: 1477-9129 , 0950-1991
    URL: Article
    DOI: 10.1242/dev.079970
    Language: English
    Publisher: The Company of Biologists
    Publication Date: 2012
    detail.hit.zdb_id: 2007916-3
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Resolvin D Series and Protectin D1 Mitigate Acute Kidney Injury
    The American Association of Immunologists ; 2006
    In:  The Journal of Immunology Vol. 177, No. 9 ( 2006-11-01), p. 5902-5911
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 177, No. 9 ( 2006-11-01), p. 5902-5911
    Abstract: Omega-3 fatty acid docosahexaenoic acid is converted to potent resolvins (Rv) and protectin D1 (PD1), two newly identified families of natural mediators of resolution of inflammation. We report that, in response to bilateral ischemia/reperfusion injury, mouse kidneys produce D series resolvins (RvDs) and PD1. Administration of RvDs or PD1 to mice before the ischemia resulted in a reduction in functional and morphological kidney injury. Initiation of RvDs and RvD1 administration 10 min after reperfusion also resulted in protection of the kidney as measured by serum creatinine 24 and 48 h later. Interstitial fibrosis after ischemia/reperfusion was reduced in mice treated with RvDs. Both RvDs and PD1 reduced the number of infiltrating leukocytes and blocked TLR-mediated activation of macrophages. Thus, the renal production of Rv and protectins, a previously unrecognized endogenous anti-inflammatory response, may play an important role in protection against and resolution of acute kidney injury. These data may also have therapeutic implications for potentiation of recovery from acute kidney injury.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.177.9.5902
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2006
    detail.hit.zdb_id: 1475085-5
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  • 4
    Online Resource
    Online Resource
    Kidney-resident macrophages promote a proangiogenic environment in the normal and chronically ischemic mouse kidney
    Springer Science and Business Media LLC ; 2018
    In:  Scientific Reports Vol. 8, No. 1 ( 2018-09-17)
    Details
    In: Scientific Reports, Springer Science and Business Media LLC, Vol. 8, No. 1 ( 2018-09-17)
    Abstract: Renal artery stenosis (RAS) caused by narrowing of arteries is characterized by microvascular damage. Macrophages are implicated in repair and injury, but the specific populations responsible for these divergent roles have not been identified. Here, we characterized murine kidney F4/80 + CD64 + macrophages in three transcriptionally unique populations. Using fate-mapping and parabiosis studies, we demonstrate that CD11b/c int are long-lived kidney-resident (KRM) while CD11c hi Mϕ, CD11c lo Mϕ are monocyte-derived macrophages. In a murine model of RAS, KRM self-renewed, while CD11c hi Mϕ and CD11c lo Mϕ increased significantly, which was associated with loss of peritubular capillaries. Replacing the native KRM with monocyte-derived KRM using liposomal clodronate and bone marrow transplantation followed by RAS, amplified loss of peritubular capillaries. To further elucidate the nature of interactions between KRM and peritubular endothelial cells, we performed RNA-sequencing on flow-sorted macrophages from Sham and RAS kidneys. KRM showed a prominent activation pattern in RAS with significant enrichment in reparative pathways, like angiogenesis and wound healing. In culture, KRM increased proliferation of renal peritubular endothelial cells implying direct pro-angiogenic properties. Human homologs of KRM identified as CD11b int CD11c int CD68 + increased in post-stenotic kidney biopsies from RAS patients compared to healthy human kidneys, and inversely correlated to kidney function. Thus, KRM may play protective roles in stenotic kidney injury through expansion and upregulation of pro-angiogenic pathways.
    Type of Medium: Online Resource
    ISSN: 2045-2322
    URL: Article
    DOI: 10.1038/s41598-018-31887-4
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2018
    detail.hit.zdb_id: 2615211-3
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  • 5
    Online Resource
    Online Resource
    Inhibition of αvβ5 Integrin Attenuates Vascular Permeability and Protects against Renal Ischemia-Reperfusion Injury
    Ovid Technologies (Wolters Kluwer Health) ; 2017
    In:  Journal of the American Society of Nephrology Vol. 28, No. 6 ( 2017-6), p. 1741-1752
    Details
    In: Journal of the American Society of Nephrology, Ovid Technologies (Wolters Kluwer Health), Vol. 28, No. 6 ( 2017-6), p. 1741-1752
    Abstract: Ischemia-reperfusion injury (IRI) is a leading cause of AKI. This common clinical complication lacks effective therapies and can lead to the development of CKD. The α v β 5 integrin may have an important role in acute injury, including septic shock and acute lung injury. To examine its function in AKI, we utilized a specific function-blocking antibody to inhibit α v β 5 in a rat model of renal IRI. Pretreatment with this anti- α v β 5 antibody significantly reduced serum creatinine levels, diminished renal damage detected by histopathologic evaluation, and decreased levels of injury biomarkers. Notably, therapeutic treatment with the α v β 5 antibody 8 hours after IRI also provided protection from injury. Global gene expression profiling of post-ischemic kidneys showed that α v β 5 inhibition affected established injury markers and induced pathway alterations previously shown to be protective. Intravital imaging of post-ischemic kidneys revealed reduced vascular leak with α v β 5 antibody treatment. Immunostaining for α v β 5 in the kidney detected evident expression in perivascular cells, with negligible expression in the endothelium. Studies in a three-dimensional microfluidics system identified a pericyte-dependent role for α v β 5 in modulating vascular leak. Additional studies showed α v β 5 functions in the adhesion and migration of kidney pericytes in vitro . Initial studies monitoring renal blood flow after IRI did not find significant effects with α v β 5 inhibition; however, future studies should explore the contribution of vasomotor effects. These studies identify a role for α v β 5 in modulating injury-induced renal vascular leak, possibly through effects on pericyte adhesion and migration, and reveal α v β 5 inhibition as a promising therapeutic strategy for AKI.
    Type of Medium: Online Resource
    ISSN: 1046-6673 , 1533-3450
    URL: Article
    DOI: 10.1681/ASN.2016020200
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2017
    detail.hit.zdb_id: 2029124-3
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  • 6
    Online Resource
    Online Resource
    The mesenchymal stem cell marker CD248 (endosialin) is a negative regulator of bone formation in mice
    Wiley ; 2012
    In:  Arthritis & Rheumatism Vol. 64, No. 10 ( 2012-10), p. 3334-3343
    Details
    In: Arthritis & Rheumatism, Wiley, Vol. 64, No. 10 ( 2012-10), p. 3334-3343
    Type of Medium: Online Resource
    ISSN: 0004-3591
    URL: Article
    DOI: 10.1002/art.34556
    RVK:
    XA 10000
    RVK:
    XA 30325
    Language: English
    Publisher: Wiley
    Publication Date: 2012
    detail.hit.zdb_id: 2754614-7
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  • 7
    Online Resource
    Online Resource
    Pericytes and immune cells contribute to complement activation in tubulointerstitial fibrosis
    American Physiological Society ; 2017
    In:  American Journal of Physiology-Renal Physiology Vol. 312, No. 3 ( 2017-03-01), p. F516-F532
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 312, No. 3 ( 2017-03-01), p. F516-F532
    Abstract: We have examined the pathogenic role of increased complement expression and activation during kidney fibrosis. Here, we show that PDGFRβ-positive pericytes isolated from mice subjected to obstructive or folic acid injury secrete C1q. This was associated with increased production of proinflammatory cytokines, extracellular matrix components, collagens, and increased Wnt3a-mediated activation of Wnt/β-catenin signaling, which are hallmarks of myofibroblast activation. Real-time PCR, immunoblots, immunohistochemistry, and flow cytometry analysis performed in whole kidney tissue confirmed increased expression of C1q, C1r, and C1s as well as complement activation, which is measured as increased synthesis of C3 fragments predominantly in the interstitial compartment. Flow studies localized increased C1q expression to PDGFRβ-positive pericytes as well as to CD45-positive cells. Although deletion of C1qA did not prevent kidney fibrosis, global deletion of C3 reduced macrophage infiltration, reduced synthesis of C3 fragments, and reduced fibrosis. Clodronate mediated depletion of CD11bF4/80 high macrophages in UUO mice also reduced complement gene expression and reduced fibrosis. Our studies demonstrate local synthesis of complement by both PDGFRβ-positive pericytes and CD45-positive cells in kidney fibrosis. Inhibition of complement activation represents a novel therapeutic target to ameliorate fibrosis and progression of chronic kidney disease.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00604.2016
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2017
    detail.hit.zdb_id: 1477287-5
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  • 8
    Online Resource
    Online Resource
    Activated Macrophages Direct Apoptosis and Suppress Mitosis of Mesangial Cells
    The American Association of Immunologists ; 2000
    In:  The Journal of Immunology Vol. 164, No. 4 ( 2000-02-15), p. 2110-2119
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 164, No. 4 ( 2000-02-15), p. 2110-2119
    Abstract: During inflammation in the glomerulus, the complement of resident myofibroblast-like mesangial cells is regulated by mitosis and apoptosis, but the cellular mechanisms controlling the size of mesangial cell populations have remained obscure. Prompted by studies of development, we sought evidence that macrophages regulate mesangial cell number. Rat bone marrow-derived macrophages primed with IFN-γ then further activated in coculture with LPS or TNF-α elicited a 10-fold induction of rat mesangial cell apoptosis and complete suppression of mitosis, effects inhibitable by the NO synthase inhibitors l-monomethyl arginine and l-N6-(1-iminoethyl) lysine dihydrochloride. Complete dependence upon macrophage-derived NO was observed in comparable experiments employing activated bone marrow macrophages from wild-type and NO synthase 2−/− mice. Nevertheless, when mesangial cells were primed with IFN-γ plus TNF-α, increased induction by activated macrophages of mesangial apoptosis exhibited a NO-independent element. The use of gld/gld macrophages excluded a role for Fas ligand in this residual kill, despite increased expression of Fas and increased susceptibility to soluble Fas ligand exhibited by cytokine-primed mesangial cells. Finally, activated macrophages isolated from the glomeruli of rats with nephrotoxic nephritis also induced apoptosis and suppressed mitosis in mesangial cells by an l-monomethyl arginine-inhibitable mechanism. These data demonstrate that activated macrophages, via the release of NO and other mediators, regulate mesangial cell populations in vitro and may therefore control the mesangial cell complement at inflamed sites.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.164.4.2110
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2000
    detail.hit.zdb_id: 1475085-5
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  • 9
    Online Resource
    Online Resource
    TWEAK-Fn14 Signaling Activates Myofibroblasts to Drive Progression of Fibrotic Kidney Disease
    Ovid Technologies (Wolters Kluwer Health) ; 2016
    In:  Journal of the American Society of Nephrology Vol. 27, No. 12 ( 2016-12), p. 3639-3652
    Details
    In: Journal of the American Society of Nephrology, Ovid Technologies (Wolters Kluwer Health), Vol. 27, No. 12 ( 2016-12), p. 3639-3652
    Abstract: The identification of the cellular origins of myofibroblasts has led to the discovery of novel pathways that potentially drive myofibroblast perpetuation in disease. Here, we further investigated the role of innate immune signaling pathways in this process. In mice, renal injury-induced activation of pericytes, which are myofibroblast precursors attached to endothelial cells, led to upregulated expression of TNF receptor superfamily member 12a, also known as fibroblast growth factor-inducible 14 (Fn14), by these cells. In live rat kidney slices, administration of the Fn14 ligand, TNF-related weak inducer of apoptosis (TWEAK), promoted pericyte-dependent vasoconstriction followed by pericyte detachment from capillaries. In vitro , administration of TWEAK activated and differentiated pericytes into cytokine-producing myofibroblasts, and further activated established myofibroblasts in a manner requiring canonical and noncanonical NF- κ B signaling pathways. Deficiency of Fn14 protected mouse kidneys from fibrogenesis, inflammation, and associated vascular instability after in vivo injury, and was associated with loss of NF- κ B signaling. In a genetic model of spontaneous CKD, therapeutic delivery of anti-TWEAK blocking antibodies attenuated disease progression, preserved organ function, and increased survival. These results identify the TWEAK-Fn14 signaling pathway as an important factor in myofibroblast perpetuation, fibrogenesis, and chronic disease progression.
    Type of Medium: Online Resource
    ISSN: 1046-6673 , 1533-3450
    URL: Article
    DOI: 10.1681/ASN.2015111227
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2016
    detail.hit.zdb_id: 2029124-3
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  • 10
    Online Resource
    Online Resource
    Lung pericyte-like cells are functional interstitial immune sentinel cells
    American Physiological Society ; 2017
    In:  American Journal of Physiology-Lung Cellular and Molecular Physiology Vol. 312, No. 4 ( 2017-04-01), p. L556-L567
    Details
    In: American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 312, No. 4 ( 2017-04-01), p. L556-L567
    Abstract: Pericytes are perivascular PDGF receptor-β + (PDGFRβ + ) stromal cells required for vasculogenesis and maintenance of microvascular homeostasis in many organs. Because of their unique juxtaposition to microvascular endothelium, lung PDGFRβ + cells are well situated to detect proinflammatory molecules released following epithelial injury and promote acute inflammatory responses. Thus we hypothesized that these cells represent an unrecognized immune surveillance or injury-sentinel interstitial cell. To evaluate this hypothesis, we isolated PDGFRβ + cells from murine lung and demonstrated that they have characteristics consistent with a pericyte population (referred to as pericyte-like cells for simplicity hereafter). We showed that pericyte-like cells expressed functional Toll-like receptors and upregulated chemokine expression following exposure to bronchoalveolar lavage fluid (BALF) collected from mice with sterile lung injury. Interestingly, BALF from mice without lung injury also induced chemokine expression in pericyte-like cells, suggesting that pericyte-like cells are primed to sense epithelial injury (permeability changes). Following LPS-induced lung inflammation, increased numbers of pericyte-like cells expressed IL-6, chemokine (C-X-C motif) ligand-1, chemokine (C-C motif) ligand 2/ monocyte chemotactic protein-1, and ICAM-1 in vivo. Sterile lung injury in pericyte-ablated mice was associated with decreased inflammation compared with normal mice. In summary, we found that pericyte-like cells are immune responsive and express diverse chemokines in response to lung injury in vitro and in vivo. Furthermore, pericyte-like cell ablation attenuated inflammation in sterile lung injury, suggesting that these cells play an important functional role in mediating lung inflammatory responses. We propose a model in which pericyte-like cells function as interstitial immune sentinels, detecting proinflammatory molecules released following epithelial barrier damage and participating in recruitment of circulating leukocytes.
    Type of Medium: Online Resource
    ISSN: 1040-0605 , 1522-1504
    URL: Article
    DOI: 10.1152/ajplung.00349.2016
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2017
    detail.hit.zdb_id: 1477300-4
    SSG: 12
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