Chondromodulin-I maintains cardiac valvular function by preventing angiogenesis

Yoshioka, Masatoyo; Yuasa, Shinsuke; Matsumura, Keisuke; Kimura, Kensuke; Shiomi, Takayuki; Kimura, Naritaka; Shukunami, Chisa; Okada, Yasunori; Mukai, Makio; Shin, Hankei; Yozu, Ryohei; Sata, Masataka; Ogawa, Satoshi; Hiraki, Yuji; Fukuda, Keiichi

doi:10.1038/nm1476

Cited by 137 publications

(119 citation statements)

References 42 publications

Supporting

Mentioning

107

Contrasting

Unclassified

Order By: Relevance

“…See electronic supplementary material, figure S1 in appendix A, for immunofluorescent staining of the leaflet endothelium. In figure 3c, leaflet Chm1 expression, associated with anti-angiogenic activity [42], was decreased in the 13% oxygen mitral leaflet group. In figure 3d, the 13% oxygen mitral leaflet group showed an increase in RUNX2, the upregulation of which is associated with myxomatous disease progression in mitral valves [17].…”

Section: Mitral Valve Leaflets Show Altered Pro-and Antiangiogenic Famentioning

confidence: 93%

Differential cell-matrix responses in hypoxia-stimulated aortic versus mitral valves

Sapp¹,

Krishnamurthy²,

Puperi³

et al. 2016

J. R. Soc. Interface.

View full text Add to dashboard Cite

Tissue oxygenation often plays a significant role in disease and is an essential design consideration for tissue engineering. Here, oxygen diffusion profiles of porcine aortic and mitral valve leaflets were determined using an oxygen diffusion chamber in conjunction with computational models. Results from these studies revealed the differences between aortic and mitral valve leaflet diffusion profiles and suggested that diffusion alone was insufficient for normal oxygen delivery in mitral valves. During fibrotic valve disease, leaflet thickening due to abnormal extracellular matrix is likely to reduce regional oxygen availability. To assess the impact of low oxygen levels on valve behaviour, whole leaflet organ cultures were created to induce leaflet hypoxia. These studies revealed a loss of layer stratification and elevated levels of hypoxia inducible factor 1-alpha in both aortic and mitral valve hypoxic groups. Mitral valves also exhibited altered expression of angiogenic factors in response to low oxygen environments when compared with normoxic groups. Hypoxia affected aortic and mitral valves differently, and mitral valves appeared to show a stenotic, rheumatic phenotype accompanied by significant cell death. These results indicate that hypoxia could be a factor in mid to late valve disease progression, especially with the reduction in chondromodulin-1 expression shown by hypoxic mitral valves.

show abstract

Section: Mitral Valve Leaflets Show Altered Pro-and Antiangiogenic Famentioning

confidence: 93%

Differential cell-matrix responses in hypoxia-stimulated aortic versus mitral valves

Sapp¹,

Krishnamurthy²,

Puperi³

et al. 2016

J. R. Soc. Interface.

View full text Add to dashboard Cite

show abstract

“…These include cartilage, heart valves, and in the eye cornea, vitreous and lens. [15][16][17][18] In these tissues, mechanisms are in place to inhibit ingrowth of blood vessels. To maintain what has been termed the 'angiogenic privilege' in the cornea, a delicate balance exists between pro-and antiangiogenic factors (Figure 2).…”

Section: Corneal Avascularity Is the Results Of An Active Regulatory Pmentioning

confidence: 99%

Emerging techniques to treat corneal neovascularisation

Menzel‐Severing

2011

Eye

View full text Add to dashboard Cite

Neovascularisation is a major cause of visual loss in a number of ophthalmic diseases. This review aims to outline the basic regulators of vessel growth in corneal neovascularisation. An understanding of the underlying principles of physiological and pathophysiological vascular development helps to appreciate current approaches to prevent or treat corneal neovascularisation. Options for future interventions will be discussed in the light of recent evidence provided by animal models of corneal neovascularisation.

show abstract

“…Так, фактор роста сосудистого эндотелия VEGF и его два рецептора Flt1 и Klk1 ассоциированы с процессами неореваскуляризации в АК при АС [57,58]. Oстеонектин (или SPARC), секретируемый белок, участвующий в процессах неореваскуляризации и воспаления (активирует ММР 9) также экспресси-руется в АК при АС [59], экспрессия хондромодулина I -антагониста процессов неореваскуляризации, снижена при АС [60]. Активация неоангиогенеза при АС находится в сильной взаимосвязи с процессами воспаления: в исследованиях неоднократно было замечено повышение уровня экспрессии проангио-генных биомаркеров локально в месте участков вос-паления, также была выявлена способность прово-спалительного цитокина TNF-α усиливать секрецию VEGF [61].…”

Section: кальциевый обменunclassified