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Related Concept Videos

Diabetic Nephropathy01:28

Diabetic Nephropathy

Definition Diabetic nephropathy is a chronic kidney complication that results from prolonged hyperglycemia.Prevalence It is the most common cause of chronic kidney disease (CKD) and end-stage renal disease (ESRD) worldwide, affecting up to half of individuals with diabetes.Pathophysiology • Sustained hyperglycemia triggers multiple hemodynamic and metabolic changes in the kidney. • Early in the disease, increased renal blood flow and glomerular hyperfiltration occur due to afferent arteriolar...
Type IV Collagen of Basal Lamina01:05

Type IV Collagen of Basal Lamina

Type IV collagen is a 400 nm long, network-forming collagen that acts as a barrier between the epithelial and endothelial cells. Type IV collagen  forms the backbone of the basement membrane by scaffolding with laminin, entactin, proteoglycans, and fibronectin. Apart from rendering structural support to the basement membrane, it also helps entail signaling potentials necessary for both pathological and physiological functions.
A type IV collagen molecule has six alpha chains which can exist in...
Type I Diabetes II: Pathophysiology01:26

Type I Diabetes II: Pathophysiology

Type 1 diabetes mellitus arises from an immune-mediated destruction of pancreatic β-cells, resulting in an absolute deficiency of insulin. This process develops in genetically susceptible individuals when autoimmunity, environmental exposures, and immunologic dysregulation converge to trigger a targeted attack on the insulin-producing cells of the pancreas. The β-cells are located within the islets of Langerhans and are essential for regulating blood glucose by facilitating cellular uptake of...
Type II Diabetes II: Pathophysiology01:24

Type II Diabetes II: Pathophysiology

PathophysiologyType 2 diabetes mellitus (T2DM ) is a chronic metabolic disorder characterized by insulin resistance and progressive pancreatic β-cell dysfunction, leading to impaired glucose homeostasis. It results from interactions among genetic predisposition, environmental factors, and metabolic stressors, such as overnutrition and a sedentary lifestyle.Insulin Resistance and Glucose DysregulationEarly T2DM involves insulin resistance in skeletal muscle, adipose tissue, and the liver.
Type I Diabetes III: Clinical Manifestations01:19

Type I Diabetes III: Clinical Manifestations

Type 1 diabetes mellitus typically presents with rapid-onset symptoms due to the body’s inability to utilize glucose in the absence of insulin. Since insulin is required for glucose uptake into cells, its deficiency leads to hyperglycemia and cellular energy deprivation, resulting in characteristic clinical features.Polyuria and PolydipsiaOne of the earliest, most prominent symptoms is polyuria (excessive urination). When blood glucose concentrations rise above the renal threshold, the kidneys...
Pathophysiology of Diabetes01:20

Pathophysiology of Diabetes

Diabetes mellitus is a chronic metabolic disorder characterized by hyperglycemia. The four categories of diabetes are type 1 diabetes, type 2 diabetes, other specific types of diabetes, and gestational diabetes.
Type 1 diabetes is characterized by autoimmune-mediated destruction of pancreatic β cells, with environmental factors potentially triggering this process in genetically susceptible individuals. Despite many not having a family history, certain genes increase susceptibility, suggesting a...

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Related Experiment Video

Updated: Jul 11, 2026

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
07:52

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy

Published on: November 7, 2017

Collagen type VIII expression in human diabetic nephropathy.

J Gerth1, C D Cohen, U Hopfer

  • 1University of Jena, Jena, Germany.

European Journal of Clinical Investigation
|September 25, 2007
PubMed
Summary

Collagen type VIII is significantly upregulated in diabetic nephropathy, unlike other kidney diseases. This specific increase in collagen type VIII may drive diabetic nephropathy's progression by influencing cell proliferation and migration.

Related Experiment Videos

Last Updated: Jul 11, 2026

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy
07:52

A Mouse 5/6th Nephrectomy Model That Induces Experimental Uremic Cardiomyopathy

Published on: November 7, 2017

Area of Science:

  • Nephrology
  • Molecular Biology
  • Biochemistry

Background:

  • Collagen type VIII, a short-chain collagen, potentially influences cell migration, proliferation, and adherence.
  • Limited data exists on collagen type VIII expression in human diabetic nephropathy.

Purpose of the Study:

  • To investigate collagen type VIII (COL8A1 and COL8A2) mRNA and protein expression in human kidney biopsies.
  • To compare expression patterns in diabetic nephropathy versus normal kidneys, benign nephrosclerosis, and focal-segmental glomerulosclerosis.

Main Methods:

  • Retrospective analysis of 20 diabetic nephropathy biopsies, 16 benign nephrosclerosis, 9 FSGS, and 10 normal kidney biopsies.
  • Real-time PCR used to quantify COL8A1 and COL8A2 mRNA expression in glomerular and tubular compartments.
  • Immunohistochemistry and Western blotting employed to assess collagen type VIII protein levels and antibody specificity.

Main Results:

  • Significant induction of COL8A1 and COL8A2 mRNA was observed in both glomerular and tubular compartments of diabetic nephropathy kidneys.
  • COL8A1 mRNA expression was notably higher than COL8A2.
  • Increased collagen type VIII protein expression was detected in mesangial cells, tubules, and interstitium in diabetic nephropathy, with minimal staining in normal kidneys.

Conclusions:

  • Collagen type VIII upregulation is specific to diabetic nephropathy among the studied renal diseases.
  • The diabetic environment, not proteinuria or serum creatinine levels, likely drives collagen type VIII expression.
  • Elevated collagen type VIII may contribute to diabetic nephropathy pathogenesis by promoting cell proliferation and migration.