Intussusceptive capillary growth is required for glomerular repair in rat Thy-1.1 nephritis

Notoya, Mitsuru; Shinosaki, Toshihiro; Kobayashi, Tatsuo; Sakai, Tatsuo; Kurihara, Hidetake

doi:10.1046/j.1523-1755.2003.00876.x

Cited by 36 publications

(35 citation statements)

References 23 publications

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“…In agreement with previously published observations (17,22,23), glomerular RECA-1-positive capillary density was decreased at 7 d after anti-Thy1.1 antibody injection (Figure 2). Compared with the right kidney, the decrease in glomerular capillary density was significantly attenuated in the left kidneys of nephritic rats that had received CMMC infusions into the left renal artery.…”

supporting

confidence: 93%

Intrarenal Injection of Bone Marrow-Derived Angiogenic Cells Reduces Endothelial Injury and Mesangial Cell Activation in Experimental Glomerulonephritis

Uchimura

Marumo²,

Takase

et al. 2005

Journal of the American Society of Nephrology

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supporting

confidence: 93%

Intrarenal Injection of Bone Marrow-Derived Angiogenic Cells Reduces Endothelial Injury and Mesangial Cell Activation in Experimental Glomerulonephritis

Uchimura

Marumo²,

Takase

et al. 2005

Journal of the American Society of Nephrology

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“…According to Nyengaard et al (9,10), "When a new capillary is generated, a new loop in the capillary network is created corresponding to a change of exactly 1 unit, the Euler number of the network." This means that a new capillary starts as a budding out of endothelial cells through the basement membrane of an existing capillary wall or, alternatively, by intussusception (17,18). We emphasize that this definition of Nyengaard et al (9,10) differs from what has been used in some studies on glomerular capillaries in which a capillary was defined as the segment between two nodes in the network (24 -26).…”

Section: Discussionmentioning

confidence: 97%

Reversal of Glomerular Lesions Involves Coordinated Restructuring of Glomerular Microvasculature

Adamczak¹,

Gross²,

Amann³

et al. 2004

Journal of the American Society of Nephrology

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Abstract. There is increasing evidence from both human and experimental studies that at least partial reversal of glomerulosclerosis can be achieved by glomerular remodeling. This requires substantial changes in glomerular architecture, specifically of glomerular capillaries. It was the purpose of the present study to characterize the stereologic and topologic characteristics of glomerular capillaries when partial reversal of glomerular lesions is achieved by high-dose angiotensinconverting enzyme inhibitor treatment. Sham-operated male Sprague-Dawley rats were compared with subtotally nephrectomized (SNX) rats. The latter were kept untreated for 8 wk and subsequently randomly divided into one group that was continued without treatment and another group that was treated with enalapril (48 mg/kg body wt per d administered in the drinking fluid for 4 wk). Renal morphology was evaluated after 8 or 12 wk, respectively, by stereologic techniques after pressure-controlled perfusion fixation. In SNX rats at 8 and particularly at 12 wk, the glomerulosclerosis index was significantly higher than in sham-operated rats. At 12 wk, it was lower in rats that had been treated for 4 wk with enalapril compared with untreated SNX rats, suggesting partial reversal of glomerular lesions. This was associated with a decrease in mean glomerular volume and mean glomerular tuft volume, a reduced number of capillaries per glomerulus, and reduced total length of capillaries per glomerulus but without any significant change in the length of individual capillaries. The numerical capillary density (Euler number density) as an index of topologic complexity did not change. The total capillary surface area per glomerulus was strikingly increased after subtotal nephrectomy and partially reversed after enalapril. This was accounted for primarily by fewer capillaries without any change in diameter. In parallel, the number of endothelial cells per glomerulus was strikingly increased after subtotal nephrectomy and decreased with enalapril treatment, but endothelial cell volume remained elevated. The study shows harmonious coordinate remodeling of the entire glomerulus during regression of glomerular lesions after subtotal nephrectomy. Proportionate reduction of glomerular volume and capillary number without change of individual capillary length were found. The numerical capillary density of the tuft therefore remained unchanged.For a long time, the goal of therapeutic intervention in glomerular disease was to halt progression (1). More recently, it had become apparent that glomerular lesions in progressive renal diseases can be reversed to some extent presumably if there has been no major loss of podocytes. This concept was based on clinical observations of partial reversal of basal membrane thickening and mesangial expansion in diabetic patients several years after isolated pancreas transplantation (2). Furthermore, reversal of renal lesions was seen in patients with clinically cured IgA glomerulonephritis (3) as well as in experimental studies of ...

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“…In experimental situations, such as anti-Thy 1.1 mesangioproliferative glomerulonephritis (GN) in rats, glomerular capillary repair with features of angiogenesis is an integral part of the healing process (2,3), rendering this model particularly useful to identify mediators involved in glomerular capillary repair.…”

mentioning

confidence: 99%

Inducible Nitric Oxide Synthase–Derived Nitric Oxide Promotes Glomerular Angiogenesis via Upregulation of Vascular Endothelial Growth Factor Receptors

Ostendorf¹,

Roeyen²,

Westenfeld³

et al. 2004

Journal of the American Society of Nephrology

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Abstract. The vascular endothelial growth factor (VEGF) system is of major importance for glomerular endothelial repair in glomerulonephritis (GN) and is significantly affected by nitric oxide (NO) release. For investigating whether glomerular upregulation of inducible NO synthase (iNOS) in GN might affect VEGFmediated repair, a selective iNOS inhibitor, L-N6-(1-iminoethyl)-lysin (L-NIL), was administered to rats with anti-Thy 1.1 GN from day Ϫ2 until day 5 after GN induction. Compared with untreated nephritic rats, L-NIL-treated nephritic rats showed similar mean arterial BP, significantly decreased de novo peak nitrate production, and increased albuminuria on day 6. This was preceded by a significant decrease of glomerular endothelial cell proliferation and endothelial area on day 2 in L-NIL-treated nephritic rats. Upregulation of glomerular VEGF mRNA and protein expression, in particular of the VEGF 164 splicing variant, occurred similarly in L-NIL-treated and untreated nephritic rats on days 2 and 7. However, the upregulation of glomerular VEGF receptor 1 and 2 mRNA expression on day 2 was reduced by 77 and 67%, respectively, in L-NIL-treated nephritic rats as compared with untreated nephritic rats. In parallel, glomerular VEGF 165 binding was reduced by 34% in L-NIL-treated nephritic rats on day 2.

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Intussusceptive capillary growth is required for glomerular repair in rat Thy-1.1 nephritis

Abstract: Intussusceptive capillary growth, or nonsprouting angiogenesis is involved in the postinjury angiogenesis in the glomeruli, in which process mesangial cells as well as endothelial cells may play important roles.

Cited by 36 publications

References 23 publications

Intrarenal Injection of Bone Marrow-Derived Angiogenic Cells Reduces Endothelial Injury and Mesangial Cell Activation in Experimental Glomerulonephritis

Intrarenal Injection of Bone Marrow-Derived Angiogenic Cells Reduces Endothelial Injury and Mesangial Cell Activation in Experimental Glomerulonephritis

Reversal of Glomerular Lesions Involves Coordinated Restructuring of Glomerular Microvasculature

Inducible Nitric Oxide Synthase–Derived Nitric Oxide Promotes Glomerular Angiogenesis via Upregulation of Vascular Endothelial Growth Factor Receptors

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