Vasoactive Peptide-Regulated Gene Expression During Osteoblastic Differentiation

Inoue, Atsuto; Kamiya, Asako; Ishiji, Atsushi; HIROSE, Shigehisa; Hagiwara, Hiromi

doi:10.1097/00005344-200036001-00084

Cited by 6 publications

(6 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although overexpression of CNP was targeted to chondrocytes in our rescue experiments, early onset of CNP-Tg expression from the CP might have been able to affect bone metabolism at the earlier stage of skeletogenesis [17] and may have continued to affect osteoblasts or osteoclasts near the growth plate cartilage in the later stage of skeletogenesis. Whereas several in vitro effects of CNP on osteoblastic cell lineages or osteoclasts have been reported [18][19][20][21][22][23][24][25][26][27][28], the in vivo effects of CNP on bone metabolism remain elusive; and further experiments are now ongoing in our laboratory.…”

Section: Discussionmentioning

confidence: 99%

Skeletal Analysis of the Long Bone Abnormality (lbab/lbab) Mouse, A Novel Chondrodysplastic C-Type Natriuretic Peptide Mutant

et al. 2012

View full text Add to dashboard Cite

Long bone abnormality (lbab/lbab) is a strain of dwarf mice. Recent studies revealed that the phenotype is caused by a spontaneous mutation in the Nppc gene, which encodes mouse C-type natriuretic peptide (CNP). In this study, we analyzed the chondrodysplastic skeletal phenotype of lbab/lbab mice. At birth, lbab/lbab mice are only slightly shorter than their wild-type littermates. Nevertheless, lbab/lbab mice do not undergo a growth spurt, and their final body and bone lengths are only ~60% of those of wild-type mice. Histological analysis revealed that the growth plate in lbab/lbab mice, especially the hypertrophic chondrocyte layer, was significantly thinner than in wild-type mice. Overexpression of CNP in the cartilage of lbab/lbab mice restored their thinned growth plate, followed by the complete rescue of their impaired endochondral bone growth. Furthermore, the bone volume in lbab/lbab mouse was severely decreased and was recovered by CNP overexpression. On the other hand, the thickness of the growth plate of lbab/+ mice was not different from that of wild-type mice; accordingly, impaired endochondral bone growth was not observed in lbab/+ mice. In organ culture experiments, tibial explants from fetal lbab/lbab mice were significantly shorter than those from lbab/+ mice and elongated by addition of 10(-7) M CNP to the same extent as lbab/+ tibiae treated with the same dose of CNP. These results demonstrate that lbab/lbab is a novel mouse model of chondrodysplasia caused by insufficient CNP action on endochondral ossification.

show abstract

Section: Discussionmentioning

confidence: 99%

Skeletal Analysis of the Long Bone Abnormality (lbab/lbab) Mouse, A Novel Chondrodysplastic C-Type Natriuretic Peptide Mutant

et al. 2012

View full text Add to dashboard Cite

show abstract

“…It might be argued that, if osteoblasts were to differentiate closer to the vessels, bone deposition would be eccentric and not concentric with respect to the vascular framework; but this suggestion by no means explains the mechanism by which preosteoblasts "sense" the position of the vessels. Several factors may be involved, such as O 2 tension (Brighton et al 1991;Lennon et al 2001), endothelial-cell-derived cytokines (i.e., endothelin-1) (Inoue et al 2000;Kasperk et al 1997;Sasaki and Hong 1993) and growth factors (ECGF) (Canalis et al 1989;Guenther et al 1986;Streeten and Brandi 1990;Villanueva and Nimni 1990) and dendritic stromal cells connecting vascular endothelium to the bone surfaces (Palazzini et al 1998), but their precise role and mechanism of action have yet to be to defined.…”

Section: Discussionmentioning

confidence: 99%

Static and dynamic osteogenesis: two different types of bone formation

Ferretti

Palumbo

Contri

et al. 2002

Anatomy and Embryology

103

View full text Add to dashboard Cite

The onset and development of intramembranous ossification centers in the cranial vault and around the shaft of long bones in five newborn rabbits and six chick embryos were studied by light (LM) and transmission electron microscopy (TEM). Two subsequent different types of bone formation were observed. We respectively named them static and dynamic osteogenesis, because the former is characterized by pluristratified cords of unexpectedly stationary osteoblasts, which differentiate at a fairly constant distance (28+/-0.4 microm) from the blood capillaries, and the latter by the well-known typical monostratified laminae of movable osteoblasts. No significant structural and ultrastructural differences were found between stationary and movable osteoblasts, all being polarized secretory cells joined by gap junctions. However, unlike in typical movable osteoblastic laminae, stationary osteoblasts inside the cords are irregularly arranged, variously polarized and transform into osteocytes, clustered within confluent lacunae, in the same place where they differentiate. Static osteogenesis is devoted to the building of the first trabecular bony framework having, with respect to the subsequent bone apposition by typical movable osteoblasts, the same supporting function as calcified trabeculae in endochondral ossification. In conclusion, it appears that while static osteogenesis increases the bone external size, dynamic osteogenesis is mainly involved in bone compaction, i.e., in filling primary haversian spaces with primary osteons.

show abstract

“…without mechanoreceptors (Marotti, 1996;Ferretti et al 2002), thus making the mechanical strains ineffectual (likely to be already existing during static osteogenesis) since they cannot be sensed. In contrast, SO is responsive to cytokines such as endothelin I and/or vascular growth factors (ECGF) released by the endothelium (Streeten & Brandi, 1990;Villanueva & Nimni, 1990;Kasperk et al 1997;Inoue et al 2000) or by platelets (Canalis et al 1992;Chaudhary et al 2004), which are mitogens for osteoprogenitor cells. The primary function of SO is to provide a rigid scaffold containing osteocytes to DO-osteoblast laminae (Ferretti et al 2002(Ferretti et al , 2006Palumbo et al 2003Palumbo et al , 2004Marotti, 2004;Marotti et al 2010); therefore, in DO, mechanical factors can have a crucial role in transducing mechanical stresses into biological signals.…”

Section: Lindsaymentioning

confidence: 99%

“…As was demonstrated by us for the first time over the last decade in a series of structural and ultrastructural investigations, there exist two different mechanisms of bone formation, occurring in sequence during intramembranous ossification in both physiologic and pathologic conditions (Ferretti et al 2002(Ferretti et al , 2006Palumbo et al 2003Palumbo et al , 2004Marotti, 2004;Marotti et al 2010). We named these two processes of bone formation static osteogenesis (SO) and dynamic osteogenesis (DO), respectively, because the former is characterized by pluristratified cords of 'stationary' osteoblasts which differentiate by inductive stimuli (Streeten & Brandi, 1990;Villanueva & Nimni, 1990;Kasperk et al 1997;Inoue et al 2000) at a fairly constant distance from the network of blood capillaries, without moving during their transformation into osteocytes from the differentiation site; the latter being instead performed by the well-known typical monostratified laminae of 'movable' osteoblasts. The temporal sequence of events is as follows: first, variously polarized stationary osteoblasts are irregularly arranged inside cords and give rise (in the same place where they differentiate) to osteocytes clustered within confluent lacunae, thus allowing the formation of a preliminary trabecular woven bone, not valid from the mechanical viewpoint due to its too-high random cellularity.…”

Section: Introductionmentioning

confidence: 99%

PTH(1‐34) effects on repairing experimentally drilled holes in rat femur: novel aspects – qualitative vs. quantitative improvement of osteogenesis

et al. 2016

View full text Add to dashboard Cite

The timetable of effects on bone repair of the active fraction-parathyroid hormone, PTH(1-34), was analytically investigated from the morphometric viewpoint in 3-month-old male Sprague-Dawley rats, whose femurs were drilled at mid-diaphyseal level (transcortical holes). The animals were divided into groups with/without PTH(1-34) administration, and sacrificed at different times (10, 28, 45 days after surgery). The observations reported here need to be framed in the context of our previous investigations regarding bone histogenesis (Ferretti et al. Anat Embryol. 2002; 206: 21-29) in which we demonstrated the occurrence of two successive bone-forming processes during both skeletal organogenesis and bone repair, i.e. static and dynamic osteogenesis: the former (due to stationary osteoblasts, haphazardly grouped in cords) producing preliminary bad quality trabecular bone, the latter (due to typical polarized osteoblasts organized in ordered movable laminae) producing mechanically valid bone tissue. The primary function of static osteogenesis is to provide a rigid scaffold containing osteocytes (i.e. mechano-sensors) for osteoblast laminae acting in dynamic osteogenesis. In the present work, histomorphometric analysis revealed that, already 10 days after drilling, despite the holes being temporarily filled by the same amount of newly formed trabecular bone by static osteogenesis independently of the treatment, the extent of the surface of movable osteoblast-laminae (covering the trabecular surface) was statistically higher in animals submitted to PTH(1-34) administration than in control ones; this datum strongly suggests the effect of PTH(1-34) alone in anticipating the occurrence of dynamic osteogenesis involved in the production of good quality bone (with more ordered collagen texture) more suitable for loading. This study could be crucial in further translational clinical research in humans for defining the best therapeutic strategies to be applied in recovering severe skeletal lesions, particularly as regards the time of PTH(1-34) administration.

show abstract

Vasoactive Peptide-Regulated Gene Expression During Osteoblastic Differentiation

Cited by 6 publications

References 0 publications

Skeletal Analysis of the Long Bone Abnormality (lbab/lbab) Mouse, A Novel Chondrodysplastic C-Type Natriuretic Peptide Mutant

Skeletal Analysis of the Long Bone Abnormality (lbab/lbab) Mouse, A Novel Chondrodysplastic C-Type Natriuretic Peptide Mutant

Static and dynamic osteogenesis: two different types of bone formation

PTH(1‐34) effects on repairing experimentally drilled holes in rat femur: novel aspects – qualitative vs. quantitative improvement of osteogenesis

Contact Info

Product

Resources

About