[Frontiers in Bioscience, 2, d592-595, December 1, 1997]

	[Frontiers in Bioscience, 2, d592-595, December 1, 1997] Reprints PubMed CAVEAT LECTOR
	CELLULAR SIGNALING IN THE BLADDER Laurence S. Baskin^1,3, Simon W. Hayward^1,2, Ronald A. Sutherland¹, Michael S. DiSandro¹, Axel A.Thomson² and Gerald R. Cunha^1,2 Department of Urology1, Anatomy2 and Pediatrics3 University of California, San Francisco San Francisco, California, 94143-0738 Received 11/13/97 Accepted 11/25/97 3. GROWTH FACTORS If diffusable growth factors play a role in smooth muscle differentiation, one would expect to see differences in their expression during development. We therefore utilized RNAse protection assays for a panel of growth factors at strategic times during bladder development and smooth muscle differentiation (4). Specifically, we examined bladders at the embryonic stage before smooth muscle development, (14 days gestation), at the time of first smooth muscle differentiation, (16 days gestation), and then at subsequent time points, 18 days gestation, newborn, 20 days postnatally, and in adulthood. We quantified growth factors that have known differentiation properties in other organ systems. Specifically, we assessed transcripts for KGF and the KGF receptor, TGF alpha and EGF receptor, and the TGF beta family. We found that TGF beta 2 and 3 are regulated as a function of development, being expressed at a high level in early gestation and then decreasing as a function of time. TGF alpha and KGF were expressed in opposite fashion, being minimally expressed in the embryonic period with a greater expression in the mature bladder. We then created a model of bladder outlet obstruction in the rodent in order to study the effect of obstruction on smooth muscle remodeling (5). This resulted in a six-fold increase in bladder volume and a five-fold increase in bladder weight, as well as a doubling of smooth muscle cell diameter. The mRNA for the growth factor TGF beta 2 increased two-fold, TGF beta 3 increased five-fold. The mRNA for TGF alpha was elevated ten-fold. In contrast, the transcripts for KGF and the receptors for KGF and EGF did not exhibit any changes. TGF betas are known to affect extracellular matrix synthesis, and it may be that the changes in the bladder wall and increased matrix deposition resulted from the up-regulation of these growth factors.

[Frontiers in Bioscience, 2, d592-595, December 1, 1997]
Reprints
PubMed
CAVEAT LECTOR

CELLULAR SIGNALING IN THE BLADDER

Laurence S. Baskin^1,3, Simon W. Hayward^1,2, Ronald A. Sutherland¹, Michael S. DiSandro¹, Axel A.Thomson² and Gerald R. Cunha^1,2

Department of Urology1, Anatomy2 and Pediatrics3 University of California, San Francisco San Francisco, California, 94143-0738

Received 11/13/97 Accepted 11/25/97

3. GROWTH FACTORS

If diffusable growth factors play a role in smooth muscle differentiation, one would expect to see differences in their expression during development. We therefore utilized RNAse protection assays for a panel of growth factors at strategic times during bladder development and smooth muscle differentiation (4). Specifically, we examined bladders at the embryonic stage before smooth muscle development, (14 days gestation), at the time of first smooth muscle differentiation, (16 days gestation), and then at subsequent time points, 18 days gestation, newborn, 20 days postnatally, and in adulthood. We quantified growth factors that have known differentiation properties in other organ systems. Specifically, we assessed transcripts for KGF and the KGF receptor, TGF alpha and EGF receptor, and the TGF beta family. We found that TGF beta 2 and 3 are regulated as a function of development, being expressed at a high level in early gestation and then decreasing as a function of time. TGF alpha and KGF were expressed in opposite fashion, being minimally expressed in the embryonic period with a greater expression in the mature bladder. We then created a model of bladder outlet obstruction in the rodent in order to study the effect of obstruction on smooth muscle remodeling (5). This resulted in a six-fold increase in bladder volume and a five-fold increase in bladder weight, as well as a doubling of smooth muscle cell diameter. The mRNA for the growth factor TGF beta 2 increased two-fold, TGF beta 3 increased five-fold. The mRNA for TGF alpha was elevated ten-fold. In contrast, the transcripts for KGF and the receptors for KGF and EGF did not exhibit any changes. TGF betas are known to affect extracellular matrix synthesis, and it may be that the changes in the bladder wall and increased matrix deposition resulted from the up-regulation of these growth factors.