Size homeostasis is a property of both dividing and non-dividing cells. Proliferating cells double in size each mitotic cell cycle, so that daughter cells are neither bigger now smaller on average then their parents. Conversely, growth slows or stops when cells exit the division cycle and become quiescent or post-mitotic. Size homeostasis requires active coordination of growth with division. In actively proliferating cells, division would outstrip growth unless the chromosome cycle (DNA replication and mitosis) were constrained by a required (checkpoint) for adequate growth. Similarly exit from the cell cycle must be accompanied by pathways that not only stop the duplication of chromosomes but all other cellular constituents as well. In pathologic states of cellular hypertrophy, including kidney disease where cell hypertrophy is maladaptive, these processes are uncoupled so that cell growth continues under conditions were cell proliferation hs stopped. The molecular pathways that couple the chromosome cycle to cell growth are not understood. In this application we propose to explore these pathways and identify the molecular that link cell growth to cell proliferation. We will use this information to study how these pathways go awry in pathologic states of cellular hypertrophy and hyperplasia.
| Liu, Gang; Changsirikulchai, Siribha; Hudkins, Kelly L et al. (2008) Identification of platelet-derived growth factor D in human chronic allograft nephropathy. Hum Pathol 39:393-402 |
| Petermann, Arndt T; Pippin, Jeffrey; Durvasula, Raghu et al. (2005) Mechanical stretch induces podocyte hypertrophy in vitro. Kidney Int 67:157-66 |
| Vaughan, Michael R; Pippin, Jeffrey W; Griffin, Sian V et al. (2005) ATRA induces podocyte differentiation and alters nephrin and podocin expression in vitro and in vivo. Kidney Int 68:133-44 |
| Griffin, Sian V; Krofft, Ronald D; Pippin, Jeffrey W et al. (2005) Limitation of podocyte proliferation improves renal function in experimental crescentic glomerulonephritis. Kidney Int 67:977-86 |
| Petermann, Arndt T; Pippin, Jeffrey; Krofft, Ron et al. (2004) Viable podocytes detach in experimental diabetic nephropathy: potential mechanism underlying glomerulosclerosis. Nephron Exp Nephrol 98:e114-23 |
| Rodriguez-Iturbe, Bernardo; Vaziri, Nosratola D; Herrera-Acosta, Jaime et al. (2004) Oxidative stress, renal infiltration of immune cells, and salt-sensitive hypertension: all for one and one for all. Am J Physiol Renal Physiol 286:F606-16 |
| Griffin, Sian V; Hiromura, Keiju; Pippin, Jeffrey et al. (2004) Cyclin-dependent kinase 5 is a regulator of podocyte differentiation, proliferation, and morphology. Am J Pathol 165:1175-85 |
| Cybulsky, Andrey V; Takano, Tomoko; Papillon, Joan et al. (2004) Renal expression and activity of the germinal center kinase SK2. Am J Physiol Renal Physiol 286:F16-25 |
| Durvasula, Raghu V; Petermann, Arndt T; Hiromura, Keiju et al. (2004) Activation of a local tissue angiotensin system in podocytes by mechanical strain. Kidney Int 65:30-9 |
| Hudkins, Kelly L; Gilbertson, Debra G; Carling, Matthew et al. (2004) Exogenous PDGF-D is a potent mesangial cell mitogen and causes a severe mesangial proliferative glomerulopathy. J Am Soc Nephrol 15:286-98 |
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