Podocyte

Source: Wikipedia, the free encyclopedia.

Podocyte
Renal corpuscle structure Blood flows in the afferent arteriole at the top, and out the efferent arteriole at the bottom. Blood flows through the capillaries of the glomerulus, where it is filtered by pressure. The podocytes (green) are wrapped around the capillaries. Blood is filtered through the slit diaphragm (or filtration slit), between the feet or processes of the podocytes. The filtered blood passes out the proximal tubule (yellow) on the right.
Details
PrecursorIntermediate mesoderm
LocationBowman's capsule of the kidney
Identifiers
Latinpodocytus
MeSHD050199
FMA70967
Anatomical terms of microanatomy

Podocytes are

viscera have epithelial
layers, the name visceral epithelial cells usually refers specifically to podocytes, which are specialized epithelial cells that reside in the visceral layer of the capsule.

The podocytes have long foot processes called pedicels, for which the cells are named (podo- + -cyte). The pedicels wrap around the capillaries and leave slits between them. Blood is filtered through these slits, each known as a filtration slit, slit diaphragm, or slit pore.[2] Several proteins are required for the pedicels to wrap around the capillaries and function. When infants are born with certain defects in these proteins, such as nephrin and CD2AP, their kidneys cannot function. People have variations in these proteins, and some variations may predispose them to kidney failure later in life. Nephrin is a zipper-like protein that forms the slit diaphragm, with spaces between the teeth of the zipper big enough to allow sugar and water through but too small to allow proteins through. Nephrin defects are responsible for congenital kidney failure. CD2AP regulates the podocyte cytoskeleton and stabilizes the slit diaphragm.[3][4]

Structure

Diagram showing the basic physiologic mechanisms of the kidney

Podocytes are found lining the Bowman's capsules in the nephrons of the kidney. The foot processes known as pedicels that extend from the podocytes wrap themselves around the

ultrafiltration.[5]

Pedicels of podocytes interdigitating to create numerous filtration slits around glomerular capillaries in 5000x electron micrograph

Podocytes secrete and maintain the basement membrane.[2]

There are numerous coated

vesicles
and coated pits along the basolateral domain of the podocytes which indicate a high rate of vesicular traffic.

Podocytes possess a well-developed

protein synthesis and post-translational modifications
.

There is also growing evidence of a large number of multivesicular bodies and other lysosomal components seen in these cells, indicating a high endocytic activity.

Function

Scheme of filtration barrier (blood-urine) in the kidney.
A. The endothelial cells of the glomerulus; 1. pore (fenestra).
B. Glomerular basement membrane: 1. lamina rara interna 2. lamina densa 3. lamina rara externa
C. Podocytes: 1. enzymatic and structural protein 2. filtration slit 3. diaphragma

Podocytes have primary processes called trabeculae, which wrap around the

macromolecules such as serum albumin and gamma globulin and ensure that they remain in the bloodstream.[7] Proteins that are required for the correct function of the slit diaphragm include nephrin,[8] NEPH1, NEPH2,[9] podocin, CD2AP.[10] and FAT1.[11]

The protein composition of podocytes and the slit diaphragm.

Small molecules such as

ultrafiltrate in the tubular fluid, which is further processed by the nephron to produce urine
.

Podocytes are also involved in regulation of glomerular filtration rate (GFR). When podocytes contract, they cause closure of filtration slits. This decreases the GFR by reducing the surface area available for filtration.

Clinical significance

Morphologic patterns of podocyte injury.[12]

A loss of the foot processes of the podocytes (i.e., podocyte effacement) is a hallmark of minimal change disease, which has therefore sometimes been called foot process disease.[13]

Disruption of the filtration slits or destruction of the podocytes can lead to massive proteinuria, where large amounts of protein are lost from the blood.

An example of this occurs in the congenital disorder

Finnish-type nephrosis, which is characterised by neonatal proteinuria leading to end-stage kidney failure. This disease has been found to be caused by a mutation in the nephrin
gene.

In 2002 Professor Moin Saleem at the University of Bristol made the first conditionally immortalised human podocyte cell line.[14][further explanation needed] This meant that podocytes could be grown and studied in the lab. Since then many discoveries have been made. Nephrotic syndrome occurs when there is a breakdown of the glomerular filtration barrier. The podocytes form one layer of the filtration barrier. Genetic mutations can cause podocyte dysfunction leading to an inability of the filtration barrier to restrict urinary protein loss. There are currently 53 genes known to play a role in genetic nephrotic syndrome.[15] In idiopathic nephrotic syndrome, there is no known genetic mutation. It is thought to be caused by a hitherto unknown circulating permeability factor.[16] Recent evidence suggests that the factor could be released by T-cells or B-cells,[17][18] podocyte cell lines can be treated with plasma from patients with nephrotic syndrome to understand the specific responses of the podocyte to the circulating factor. There is growing evidence that the circulating factor could be signalling to the podocyte via the PAR-1 receptor.[19][further explanation needed]

Presence of podocytes in urine has been proposed as an early diagnostic marker for

preeclampsia.[20]

See also

References

External links