PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “kidney morphogenesis”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 127 records · Page 7Linked to original sources
PubMed2005

Protein kinase X activates ureteric bud branching morphogenesis in developing mouse metanephric kidney.

The human protein kinase X (PRKX) gene was identified previously as a cAMP-dependent serine/threonine kinase that is aberrantly expressed in autosomal dominant polycystic disease kidneys and normally expressed in fetal kidneys. The PRKX kinase belongs to a serine/threonine kinase family that is phylogenetically and functionally distinct from classical protein kinase A kinases. Expression of PRKX activates cAMP-dependent renal epithelial cell migration and tubular morphogenesis in cell culture, suggesting that it might regulate branching growth of the collecting duct system in the fetal kidney. With the use of a mouse embryonic kidney organ culture system that recapitulates early kidney development in vitro, it is demonstrated that lentiviral vector-driven expression of a constitutively active, cAMP-independent PRKX in the ureteric bud epithelium stimulates branching morphogenesis and results in a 2.5-fold increase in glomerular number. These results suggest that PRKX stimulates epithelial branching morphogenesis by activating cell migration and support a role for this kinase in the regulation of nephrogenesis and of collecting system development in the fetal kidney.

Animals↗
PubMed2002

The polycystin-1 C-terminal fragment triggers branching morphogenesis and migration of tubular kidney epithelial cells.

Mutations of either PKD1 or PKD2 cause autosomal dominant polycystic kidney disease, a syndrome characterized by extensive formation of renal cysts and progressive renal failure. Homozygous deletion of Pkd1 or Pkd2, the genes encoding polycystin-1 and polycystin-2, disrupt normal renal tubular differentiation in mice but do not affect the early steps of renal development. Here, we show that expression of the C-terminal 112 amino acids of human polycystin-1 triggers branching morphogenesis and migration of inner medullary collecting duct (IMCD) cells, and support in vitro tubule formation. The integrity of the polycystin-2-binding region is necessary but not sufficient to induce branching of IMCD cells. The C-terminal domain of polycystin-1 stimulated protein kinase C-alpha (PKC-alpha), but not the extracellular signal-regulated kinases ERK1 or ERK2. Accordingly, inhibition of PKC, but not ERK, prevented polycystin-1-mediated IMCD cell morphogenesis. In contrast, HGF-mediated morphogenesis required ERK activation but was not dependent on PKC. Our findings demonstrate that the C-terminal domain of polycystin-1, acting in a ligand-independent fashion, triggers unique signaling pathways for morphogenesis, and likely plays a central role in polycystin-1 function.

Animals↗
PubMed1998

Cytomechanics of cadherin-mediated cell-cell adhesion.

Cadherin-mediated adhesion regulates transitions from initial cell-cell recognition to loosely adherent cell clusters and ultimately, to strongly compacted groups of cells in colonies. Recent studies have described distinct roles for intermolecular clustering of cadherins as well as interactions of cadherin with the actin cytoskeleton in establishing cell-cell adhesion. Integrating cytomechanical roles of cadherin-mediated adhesion will lead to a greater understanding of how cadherins regulate tissue morphogenesis.

Actins↗
PubMed2000

Advances in renal development.

Branching morphogenesis, mesenchymal cell condensation and mesenchymal-to-epithelial conversion are key steps in kidney development and morphogenesis of several other organs. Review articles describing our current knowledge of the genetic and molecular regulation of these processes have been published. Therefore, this review focuses on the important question of cell lineage specification during kidney development. We describe how new insights are being made into the specification of kidney cells in the intermediate mesoderm, as well as specification of cells that will form the renal mesenchyme, ureteric duct, nephron tubule epithelium and renal vasculature.

Animals↗
PubMed1986

[Morpho- and pathogenesis of nephrosclerosis: a clinico-morphological analysis].

The authors have defined 2 phases in morphogenesis of nephrosclerosis: "nosological" and "syndrome". In the first phase the development of nephrosclerosis is determined by the peculiarities of pathogenesis of the main disease and associated with a certain structural element of the kidney (arterioles, glomerula, stroma). The second phase occurs after the formation of block of the renal blood flow at one or another structural level (arteriolar, glomerular, capillary-parenchymatous) including the hypoxic factor which determines subsequent progression of nephrosclerosis. The nosological signs of nephrosclerosis in this phase are leveled down, replaced by the signs of the syndrome of chronic renal failure. Arterial hypertension is a factor contributing to the progression of nephrosclerosis irrespective of nosological entity.

Amyloidosis↗
PubMed1998

[Morphogenesis of the vena cava inferior roots in human embryogenesis].

The roots of the vena cava inferior are formed during the 2nd month of human embryogenesis in the course of transformation of posterior caudal veins and their tributaries, including anastomoses with umbilical veins, which is associated with the growth of pelvic kidney and lower extremities. The roots and initial part of vena cava inferior originate from secondary cardinal veins, primarily from sacrocardinal anastomosis and sacrocardinal veins proximal regions.

Embryonic and Fetal Development↗
PubMed1995

Cadherin 11 expression marks the mesenchymal phenotype: towards new functions for cadherins?

Cadherin-11 (cad-11) belongs to the cell adhesion type II cadherin family, which seems to have different functions from the classic cadherin family. This study shows the overall pattern of cad-11 gene expression during rat embryonic development, from the pregastrula to very late embryonic stage. Cad-11 is the first cadherin found to be highly expressed in the dispersed and migrating mesenchymal cells that originate from the neuroectodermal neural crest cells and from the pre-chordal and paraxial mesoderm. A burst of cad-11 expression appears during the epithelial to mesenchymal transition, as observed by sclerotome formation. Cad-11 mRNAs were present in all mesenchymal cells throughout the embryo, regardless of their embryonic origin. A proximo-distal and antero-posterior gradient of cad-11 expression is seen in the limb buds, genitalia, and tail. As development proceeds, while all epithelium are negative, cad-11 is present in all mesenchymal cells involved in various morphogenetic events, such as the mesenchyme condensations during chondrogenesis and in the formation of sclera, cornea, naris, palate and meninges. Cad-11 was strongly expressed in mesenchyme during lung or kidney branching morphogenesis or the many epithelium to mesenchyme inductions that operate in the nasal septum, skin, vibrissae, teeth and various glands. High levels of cad-11 transcripts were also found in the dispersed cells of the hyaloid plexus in the vitreous body and in the invading mesenchyme within the trabeculae of the outflow tract of the heart. Cad-11 is thus specific to the mesenchymal phenotype whatever the stage of embryonic development.

Amino Acid Sequence↗
PubMed1994

Further analysis of the effect of Ca2+ on morphogenesis of HVJ (Sendai virus) in LLC-MK2 cells: effects on phosphorylated M protein associated with viral morphogenesis.

Previously we have reported that Ca2+ concentration in culture medium affects the morphogenesis of HVJ from infected cells. We further investigated the effects of Ca2+ on HVJ morphogenesis in LLC-MK2 cells, focusing on M (matrix) protein which plays an important role in the assembly of viral components. On culture in standard medium (containing 1.8 mM Ca2+), most of the M protein accumulated on the apical surface in patches. On double immunofluorescent staining with anti-M protein monoclonal antibody and polyclonal antibody against HVJ glycoproteins, M protein and viral glycoproteins were observed in the same patches at the cell surface. By contrast, in low Ca2+ medium, M protein was evenly dispersed over the cell surface, especially in the regions of cell-cell contact, and was not seen in patches. Immunoblot analysis for M protein in the infected cells showed that the total amount of M protein was almost the same irrespective of Ca2+ concentration in the culture medium. But, there was a distinct difference in the forms of M protein found in the cells: most of the M protein in the cells cultured in standard medium was of the non-phosphorylated form, whereas the phosphorylated form of M protein was distinctly increased in the cells cultured in low Ca2+ medium. These results suggest that Ca(2+)-deficiency in the medium blocks dephosphorylation of phosphorylated M protein necessary for patch formation, resulting in disturbance of viral morphogenesis.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2002

PAX genes in development and disease: the role of PAX2 in urogenital tract development.

PAX genes play an important role in fetal development. Moreover, heterozygous mutations in several PAX genes cause human disease. Here we review the role of PAX2 in kidney development, focusing on the morphological effects of PAX2 mutations. We discuss the role of PAX2 in the context of an inhibitory field model of kidney branching morphogenesis and summarize recent progress in this area.

Animals↗