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Assessment of Kidney Function in Mouse Models of Glomerular Disease
Published on: June 30, 2018
An ACTH-induced renal glomerular lesion in the mouse: immunofluorescence microscopy
The Journal of Pathology
|March 1, 1983
Summary
Adrenocorticotropic hormone (ACTH) induced glomerular lesions in mice, increasing plasma protein accumulation in the juxtaglomerular apparatus (JGA). This suggests the JGA may play a role in clearing glomerular and blood proteins.
Area of Science:
- Nephrology
- Immunology
- Endocrinology
Background:
- Adrenocorticotropic hormone (ACTH) is known to induce glomerular lesions.
- The precise mechanisms and locations of plasma protein deposition in these lesions are not fully understood.
Purpose of the Study:
- To investigate the deposition patterns of plasma proteins, specifically immunoglobulins (IgG, IgM), complement (C3), and albumin, in ACTH-induced glomerular lesions in mice.
- To explore the potential role of the juxtaglomerular apparatus (JGA) in plasma protein handling within the kidney.
Main Methods:
- Mice were treated with ACTH to induce glomerular lesions.
- Kidney tissues were examined using light microscopy and immunofluorescence microscopy.
- Immunofluorescence staining was performed for IgG, IgM, C3, and albumin.
Main Results:
- Light microscopy confirmed typical ACTH-induced glomerular lesions.
- Immunofluorescence revealed intense IgG and IgM staining in the extraglomerular mesangium (EGM) and Bowman's space.
- Accumulation of C3 and albumin was observed in the EGM, Bowman's space, and glomerular tuft, with patterns similar but less frequent in control mice.
Conclusions:
- ACTH treatment in mice leads to increased accumulation of plasma proteins within the JGA.
- These findings suggest a potential role for the JGA in the clearance of plasma proteins from the glomerulus and/or directly from circulation.

