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Increased soluble EGF after ischemia is accompanied by a decrease in membrane-associated precursors

R P Schaudies¹, J P Johnson

¹Department of Nephrology, Walter Reed Army Institute of Research, Washington, District of Columbia 20307.

The American Journal of Physiology

|March 1, 1993

Summary

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Ischemia-injured rat kidneys show significantly increased soluble epidermal growth factor (EGF), a key growth factor. This suggests EGF release from membrane precursors promotes kidney repair after acute renal failure.

Area of Science:

Nephrology
Molecular Biology
Cellular Signaling

Background:

Acute renal failure can result from ischemia, impacting kidney function.
Epidermal growth factor (EGF) is a potent mitogen involved in cell growth and repair.

Purpose of the Study:

To investigate the distribution and forms of immunoreactive EGF (irEGF) in control and ischemia-injured rat kidneys.
To understand the role of membrane-associated EGF precursors in kidney injury recovery.

Main Methods:

Quantification of soluble and membrane-bound irEGF using radioimmunoassay.
Analysis of irEGF forms after trypsin digestion.
Affinity purification and high-performance liquid chromatography of membrane fractions.
EGF receptor binding assays and [3H]thymidine incorporation studies.

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Main Results:

Ischemia-injured kidneys exhibited a sixfold increase in soluble irEGF, primarily native and des-Arg-EGF.
Membrane-associated irEGF decreased slightly post-injury, but trypsin digestion revealed altered precursor forms.
Purified membrane fractions contained three irEGF peaks with EGF receptor binding and mitogenic activity, enhanced by trypsin digestion in two peaks.

Conclusions:

EGF is released from membrane-associated precursors following ischemic injury.
Released EGF likely promotes kidney cell growth via autocrine or paracrine mechanisms, aiding recovery from acute renal failure.