A Role of Bone Morphogenetic Proteins in Aldosterone-Induced Glomerular Injury.

2010 ◽  
pp. P3-610-P3-610
Author(s):  
J Suzuki ◽  
F Otsuka ◽  
K Inagaki ◽  
T Miyoshi ◽  
M Takeda ◽  
...  
Keyword(s):  
Bone Morphogenetic Proteins ◽  
Glomerular Injury

scholarly journals The Role of BMP Signaling in Osteoclast Regulation

2021 ◽  
Vol 9 (3) ◽  
pp. 24
Author(s):  
Brian Heubel ◽  
Anja Nohe
Keyword(s):  
Bone Formation ◽  
Bone Morphogenetic Proteins ◽  
Bone Diseases ◽  
Bmp Signaling ◽  
Bone Homeostasis ◽  
Direct Stimulation ◽  
Federal Drug Administration ◽  
Bmp Pathway ◽  
Stimulation Of

The osteogenic effects of Bone Morphogenetic Proteins (BMPs) were delineated in 1965 when Urist et al. showed that BMPs could induce ectopic bone formation. In subsequent decades, the effects of BMPs on bone formation and maintenance were established. BMPs induce proliferation in osteoprogenitor cells and increase mineralization activity in osteoblasts. The role of BMPs in bone homeostasis and repair led to the approval of BMP2 by the Federal Drug Administration (FDA) for anterior lumbar interbody fusion (ALIF) to increase the bone formation in the treated area. However, the use of BMP2 for treatment of degenerative bone diseases such as osteoporosis is still uncertain as patients treated with BMP2 results in the stimulation of not only osteoblast mineralization, but also osteoclast absorption, leading to early bone graft subsidence. The increase in absorption activity is the result of direct stimulation of osteoclasts by BMP2 working synergistically with the RANK signaling pathway. The dual effect of BMPs on bone resorption and mineralization highlights the essential role of BMP-signaling in bone homeostasis, making it a putative therapeutic target for diseases like osteoporosis. Before the BMP pathway can be utilized in the treatment of osteoporosis a better understanding of how BMP-signaling regulates osteoclasts must be established.

scholarly journals The dynamic role of bone morphogenetic proteins in neural stem cell fate and maturation

2012 ◽  
Vol 72 (7) ◽  
pp. 1068-1084 ◽  
Author(s):  
Allison M. Bond ◽  
Oneil G. Bhalala ◽  
John A. Kessler
Keyword(s):  
Stem Cell ◽  
Cell Fate ◽  
Neural Stem Cell ◽  
Bone Morphogenetic Proteins ◽  
Stem Cell Fate

Glomerular injury in end-stage liver disease — role of circulating IgG and IgM immune complexes

1993 ◽  
Vol 7 (1) ◽  
pp. 6-10 ◽  
Author(s):  
Lawrence S. Milner ◽  
Mark T. Houser ◽  
Peter C. Kolbeck ◽  
Dean L. Antonson ◽  
Thomas L. McDonald ◽  
...  
Keyword(s):  
Liver Disease ◽  
Immune Complexes ◽  
Glomerular Injury ◽  
End Stage Liver Disease ◽  
End Stage

scholarly journals The specification of noradrenergic locus coeruleus (LC) neurones depends on bone morphogenetic proteins (BMPs)

Development ◽  
2002 ◽  
Vol 129 (4) ◽  
pp. 983-991 ◽  
Author(s):  
Astrid Vogel-Höpker ◽  
Hermann Rohrer
Keyword(s):  
Transcription Factors ◽  
Locus Coeruleus ◽  
Bone Morphogenetic Proteins ◽  
Chick Embryos ◽  
Dorsal Midline ◽  
Neural Crest Development ◽  
Roof Plate ◽  
Rhombic Lip ◽  
The Brain

The role of BMPs in the development of the major noradrenergic centre of the brain, the locus coeruleus (LC), was investigated. LC generation is reflected by initial expression of the transcription factors Phox2a and Phox2b in dorsal rhombomere1 (r1), followed by expression of dopamine-β-hydroxylase and tyrosine hydroxylase. Bmp5 is expressed in the dorsal neuroepithelium in proximity to Phox2-expressing cells. BMP inhibition in stage 10 chick embryos resulted in the lack of LC neurones or in their generation at the dorsal midline, and loss of roof plate and rhombic lip, but it did not affect neural crest development. These results reveal late essential BMP functions in the specification of dorsal neuronal phenotypes in r1, including LC neurones, and in the development of dorsal midline structures.

scholarly journals The Dual Role of Bone Morphogenetic Proteins in Cancer

2018 ◽  
Vol 8 ◽  
pp. 1-13 ◽  
Author(s):  
Duc-Hiep Bach ◽  
Hyen Joo Park ◽  
Sang Kook Lee
Keyword(s):  
Bone Morphogenetic Proteins ◽  
Dual Role

scholarly journals A ROLE OF POLYMORPHONUCLEAR LEUKOCYTES AND COMPLEMENT IN NEPHROTOXIC NEPHRITIS

1965 ◽  
Vol 122 (1) ◽  
pp. 99-116 ◽  
Author(s):  
Charles G. Cochrane ◽  
Emil R. Unanue ◽  
Frank J. Dixon
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Basement Membranes ◽  
Ultrastructural Changes ◽  
Glomerular Injury ◽  
Large Numbers ◽  
Secondary Stage ◽  
Vascular Beds ◽  
Nephrotoxic Nephritis ◽  
Glomerular Damage

In acute nephrotoxic nephritis, polymorphonuclear leukocytes (polymorphs) accumulated in large numbers in the glomeruli in the first 12 hours. The endothelial cells were dislodged by the polymorphs which then came to lie immediately adjacent to the glomerular basement membranes. Ultrastructural changes in neither polymorphs nor basement membranes were observed. Depletion of polymorphs in both rats and rabbits prevented the development of proteinuria. This occurred when doses of nephrotoxic globulin were employed that produced proteinurias of as much as 1800 mg/kg/24 hours in intact rabbits, or enough to yield near maximal immediate proteinuria in intact rats. In addition, measurable glomerular damage was frequently averted until the onset of the secondary stage of NTN. Controls indicated that the polymorph depleted animals exhibited minimal non-specific changes in the blood, that the ability of their vascular beds to react to stimuli was not affected, and that deposition of nephrotoxic antibody and C' in the glomeruli was not inhibited. Elimination of polymorphs from the circulation was only partially effective in preventing glomerular damage when large doses of nephrotoxic globulin were used. This indicated that under these circumstances, a polymorph independent glomerular injury may also take place in first stage nephrotoxic nephritis. An indirect role of C', i.e., the accumulation of polymorphs, in bringing about glomerular injury in first stage nephrotoxic nephritis was apparent. When rabbit nephrotoxic globulin was injected into rats depleted of C', or when duck nephrotoxic globulin that fixed C' poorly was injected into normal rats, C' failed to bind with the antibody along glomerular basement membranes and polymorphs did not accumulate.

BMP and Ihh/PTHrP signaling interact to coordinate chondrocyte proliferation and differentiation

Development ◽  
2001 ◽  
Vol 128 (22) ◽  
pp. 4523-4534 ◽  
Author(s):  
Eleonora Minina ◽  
Hans Markus Wenzel ◽  
Conny Kreschel ◽  
Seth Karp ◽  
William Gaffield ◽  
...  
Keyword(s):  
Bone Morphogenetic Proteins ◽  
Feedback Loop ◽  
Bmp Signaling ◽  
Signaling Systems ◽  
Chondrocyte Maturation ◽  
Parathyroid Hormone Related Protein ◽  
Proliferation And Differentiation ◽  
Mouse Limb ◽  
Pthrp Expression

During endochondral ossification, two secreted signals, Indian hedgehog (Ihh) and parathyroid hormone-related protein (PTHrP), have been shown to form a negative feedback loop regulating the onset of hypertrophic differentiation of chondrocytes. Bone morphogenetic proteins (BMPs), another family of secreted factors regulating bone formation, have been implicated as potential interactors of the Ihh/PTHrP feedback loop. To analyze the relationship between the two signaling pathways, we used an organ culture system for limb explants of mouse and chick embryos. We manipulated chondrocyte differentiation by supplementing these cultures either with BMP2, PTHrP and Sonic hedgehog as activators or with Noggin and cyclopamine as inhibitors of the BMP and Ihh/PTHrP signaling systems. Overexpression of Ihh in the cartilage elements of transgenic mice results in an upregulation of PTHrP expression and a delayed onset of hypertrophic differentiation. Noggin treatment of limbs from these mice did not antagonize the effects of Ihh overexpression. Conversely, the promotion of chondrocyte maturation induced by cyclopamine, which blocks Ihh signaling, could not be rescued with BMP2. Thus BMP signaling does not act as a secondary signal of Ihh to induce PTHrP expression or to delay the onset of hypertrophic differentiation. Similar results were obtained using cultures of chick limbs. We further investigated the role of BMP signaling in regulating proliferation and hypertrophic differentiation of chondrocytes and identified three functions of BMP signaling in this process. First we found that maintaining a normal proliferation rate requires BMP and Ihh signaling acting in parallel. We further identified a role for BMP signaling in modulating the expression of Ihh. Finally, the application of Noggin to mouse limb explants resulted in advanced differentiation of terminally hypertrophic cells, implicating BMP signaling in delaying the process of hypertrophic differentiation itself. This role of BMP signaling is independent of the Ihh/PTHrP pathway.

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