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Expression of growth arrest-specific gene 6 and its receptors in dysfunctional human renal allografts
Jian L Yin1, Brett D Hambly, Shi S Bao
1Department of Renal Medicine, Royal Prince Alfred Hospital, NSW 2050, Camperdown, New South Wales, Australia.
Abstract:
Growth arrest-specific gene 6 (Gas6) and its receptors Rse, Axl and Mer have recently been found to be involved in a rat model of chronic allograft nephropathy (CAN). Thus, in this study we investigated the function of Gas6 and its receptors in human renal allograft dysfunction. Expression of Gas6 and its receptors was detected by immunohistochemical staining. Gas6 and its receptors were widely expressed in glomeruli, tubules and vessels of renal allografts. Gas6 expression was detected in normal-functioning allografts and was increased in acute rejection ( P<0.05), acute tubular necrosis ( P<0.05) and CAN ( P<0.01). Gas6 receptors were not upregulated in any of the allograft groups, except for the Axl receptor, which increased only in acute tubular necrosis ( P<0.01). Gas6 expression was also found to correspond with the expression of alpha-smooth muscle actin, a general marker of CAN ( r(2)=0.21, P<0.01). These findings suggest that Gas6, acting as a growth factor, is increased in the process of kidney allograft dysfunction and in CAN.
Insights
Growth arrest-specific gene 6 (Gas6) is elevated in human kidney allograft dysfunction and chronic allograft nephropathy (CAN). This growth factor
Area of Science:
- Nephrology
- Immunology
- Molecular Biology
Background:
- Growth arrest-specific gene 6 (Gas6) and its receptors (Axl, Mer, Rse) are implicated in rat chronic allograft nephropathy (CAN).
- The role of Gas6 signaling in human renal allograft dysfunction remains unclear.
Purpose of the Study:
- To investigate the expression and function of Gas6 and its receptors in human renal allograft dysfunction.
- To determine the correlation between Gas6 expression and markers of kidney allograft injury.
Main Methods:
- Immunohistochemical staining was used to detect Gas6 and its receptor expression in human renal allografts.
- Expression levels were compared between normal-functioning allografts and those with acute rejection, acute tubular necrosis, and CAN.
- Correlation analysis was performed between Gas6 expression and alpha-smooth muscle actin.
Main Results:
- Gas6 and its receptors were widely expressed in glomeruli, tubules, and vessels of renal allografts.
- Gas6 expression was significantly increased in acute rejection, acute tubular necrosis, and CAN compared to normal allografts.
- Axl receptor expression increased only in acute tubular necrosis; other receptors showed no significant upregulation.
- Gas6 expression positively correlated with alpha-smooth muscle actin, a marker of CAN.
Conclusions:
- Gas6 expression is upregulated in human kidney allograft dysfunction, particularly in CAN.
- Gas6 may play a role as a growth factor contributing to renal allograft injury and fibrosis.
