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Morphine modulates 72-kDa matrix metalloproteinase

S Sagar¹, D Sorbi, L A Arbeit

¹Department of Medicine, Long Island Jewish Medical Center, New Hyde Park 11042.

The American Journal of Physiology

|October 1, 1994

Summary

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Morphine exposure significantly reduces gelatinolytic activity, which degrades type IV collagen. This impaired collagen breakdown in mesangial cells may contribute to glomerulosclerosis in heroin nephropathy.

Area of Science:

Nephrology
Cell Biology
Pharmacology

Background:

Mesangial expansion is a key feature of glomerulosclerosis in heroin nephropathy.
Matrix degradation, alongside synthesis, influences mesangial expansion.
Metalloproteinases (gelatinases) degrade type IV collagen, a component of the glomerular basement membrane.

Purpose of the Study:

To investigate the effect of morphine on gelatinolytic activity in mesangial cells (MC).
To assess the in vivo impact of morphine on gelatinolytic activity in rats.

Main Methods:

Exposing MC to varying concentrations of morphine and measuring gelatinolytic activity.
Analyzing 24-hour urine and isolated glomeruli from morphine-treated rats for gelatinolytic activity.
Testing the effect of naloxone, an opioid antagonist, on morphine's impact.

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Main Results:

Morphine significantly decreased gelatinolytic activity in MC cultures at 1 and 2 weeks.
A dose-dependent reduction in gelatinolytic activity was observed with morphine (10(-10) to 10(-6) M).
In vivo studies showed reduced gelatinolytic activity in urine and glomeruli of morphine-treated rats; naloxone did not reverse this effect.

Conclusions:

Morphine reduces the activity of gelatinases that degrade type IV collagen.
This decrease in collagen degradation may lead to mesangial accumulation and expansion.
The findings suggest a mechanism linking morphine use to the progression of heroin nephropathy.