If you are educated in the mitral valve please read and review. Thanks

[JulieJones]

This info. was give to me and I am wondering if it is correct. Can someone who knows alot on the mitral valve please review it and get back to me with any comments. Thanks. Juliegkjones@hotmail.com

 

Introduction

The mitral valve ensures unidirectional blood flow through the left atrioventricular canal by preventing regurgitation of blood during ventricular systole. With this function in mind, we examined the physical changes with age in the mouse mitral valve.

The mouse mitral valve apparatus consists of, anterior and posterior papillary muscles, chordae tendinae and anterior and posterior leaflets. The papillary muscles arise from the ventricular wall near the apex of the heart and ascend up the wall. Unlike larger mammals the papillary muscles of the mouse are only independent from the ventricular wall at their tip, thereby resembling trabeculae carneae. The papillary muscles attaches directly to the valve leaflet and chordae tendinae arise close to the leaflet-muscle junction and insert into the free edge of both leaflets. Mitral valve leaflets occlude the atrioventricular orifice and seem to show no evidence of commissures or clefts. The basal portion of the leaflet attaches to the cardiac wall via the annulus of the fibroskeleton. (Icardo and Colvee, 1995a) (Icardo et al. 1993).

 

In human hearts, valve development is evident at approximately the seventh week and valves reach mature morphology at the end of the third month of gestation (Lincoln et al. 2004) (Wessels et al. 1996). The mitral valve is derived from mesenchymal endocardial cushion tissue and sulcus tissue (Wessels et al. 1996). These cushions are a pair of embryonic connective tissue masses, covered by endothelium that project dorsally and ventrally into the embryonic atrioventricular (AV) canal during heart development. (S.R. Qayyum et al. 2001), Endocardial cushions contribute a great deal to annulus and valve formation (Wessels et al. 1996). These cushions act as primitive valves during partitioning of the heart (S.R. Qayyum et al. 2001) (Oxbridge Solutions Limited, 2005). The posterior leaflet of the mitral valve is partially derived from the left lateral cushion, while the anterior leaflet is believed to be formed from the superior endocardial cushion The anterior leaflet is the first recognized leaflet to form ((Wessels et al. 1996)(Webb et al.1998)(Lincoln et al. 2004). Tissues of the endocardial cushions and sulcus fuse to become the primordia, almost completely separating the ventriclular myocardium from the atrial myocardium. (Wessels et al. 1996). After fusion of these tissues, the primordia is remodelled to form leaflets and supporting structures. Distinct extra-cellular matrix phenotypes are present in the leaflet, chordae and myotendinous junction, however the exact cell lineage is not clear (Lincoln et al 2004).

Later in month two the developing leaflets are composed of mesenchymal cells and myocytes. As the embryo grows the muscular composition of the valve seems to decrease and the valve shows a fibrous structure. The cusps increase in size due to cell proliferation and muscular degeneration beneath the valve (Lincoln et al 2004).

(Wessels et al. 1996) (Boudewijn et al. 2007).

The primitive papillary muscles are represented by elevations forming on the ventricular wall. These diverge into web-like folds which attach to the primitive valve cusps. The folds are the primordia of the chordae tendinae. Linear ridges alternating with depressions form on the folds, the depressions become perforated to create individual chorda. Several perforations form at first; these usually join to form a larger hole between chordae. Chordal development has been suggested to be a programmed cellular and haemodynamic event. (Morse et al 1984). Heart development continues postnataly for adjustment to growth in body mass and changes in vascular pressures, that occur at birth (Boudewijn et al. 2007).

The general model of a mitral valve divides the leaflet into four distinct layers, atrialis, spongiosa, fibrosa and ventricularis. The atrialis consists of endothelium and underlying collagen and elastic tissues, the endothelium is continuous with the atrial endocardial endothelium (Roberts 2005). The endocardial cells of the atrialis are plump with large irregular nuclei and thick cytoplasmic processes. The ventricular and chordal endocardial cells have flat, oval nuclei, with attenuated cytoplasmic processes (Fenoglio 1972). Small cell processes, known as microappendages, are present on the endothelial surface and form a dense covering over the cells. They increase surface area and are believed to be involved in metabolism of the cells (Hill and Folan-Curran 1993). The endothelium forms a barrier protecting underlying tissues and assists in the communication between the internal and external environment. Communication between endothelium and the environment may be accomplished via invaginations in the endothelial plasma membrane, called caveolae. These vesicular structures are considered to be a signalling trans-membrane system (Schnitzer 2001) (Anderson 1998) (Mineo and Shaul 2006). The spongiosa is loose connective tissue containing collagen fibers, elastic fibers and proteoglycans. In this layer the collagen fibers have no distinct orientation (Icardo and Colvee 1995b). Most of the thickness of the free-edge, in the mouse, is composed of the spongiosa.

The fibrosa is the supporting structure of the leaflet that contains thick undulating bands of collagen, which give rise to chordae tendinae at the free edge (Mullholand and Gotleib 1997). These collagen fibers are tightly packed and of uniform size (Icardo and Colvee 1995b).

At the free edge the atrialis becomes continuous with the ventricularis. The latter is the thinnest layer comprising mainly of elastic fibers and endothelium. The endothelium is uninterrupted with that of the chordae tendinae, into which the elastic fibres extend (Filip et al 1986).

The predominant cells types in the valve are endothelial and interstitial cells (Flanagan and Pandit 2003). Valvular interstitial cells (VICs) constitute approximately 30% of the volumetric density of the cell population in mouse atrioventricular valves (Filip et al 1986). Two basic phenotypes are recognized; a fibroblast-like cell and a smooth muscle-like cell, and an intermediate cell type can also exist. In the human valve, the fibroblast-like VICs are the predominant cell type (Black et al. 2005).

These cells lack a basal lamina, have prominent rough endoplasmic reticulum and Golgi apparatus. They also have extensive cytoplasmic processes that interact with the extra-cellular matrix (ECM) of the valve. Fibroblastic-like VICs are regarded as the primary manufacturer of the ECM and its components. Characteristics of the smooth muscle-like VICs include the ability to contract in vitro, the presence of gap junctions, actin filaments and dense bodies. This phenotype is believed to lie in close proximity to motor nerve terminals (Filip et al.1986).

VICs are contained within and secrete the extracellular matrix of the valve. In 1986, Filip et al stated that VICs are present both within the spongiosa and fibrosa but are the sole cell type of the fibrosa. The extracellular matrix contributes to the function and structure of the valve, with collagen providing valvular strength ( type I 74%, type II 24% and type V) and elastic fibers (10% of dry weight) supplying the valves extensibility (Mullholand and Gotleib 1997).

In the mouse valve, studies by Icardo and Colvee (1995) suggest that VICs are heavily involved in the secretion and degradation of collagen fibers. Regulation and remodeling of the ECM by VICs preserves the durability of the valve. Remodelling is as a result of haemodynamic forces (Black et al. 2005). VICs communicate through adherens junctions and gap junctions. These can be seen in transmission electron micrographs of smooth muscle-like VICs. However, the specific functions of these junctions have not yet been determined. As with vascular endothelium, it is most likely that the VICs are regulated by the surface endothelium, although to date this is not proven. Studies using cell culture models suggest that the endocardial endothelial cells do provide soluble growth factors mitogenic to the interstitial cells (Mullholand and Gotleib 1997) (Flanagan and Pandit 2003).

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[JulieJones]

nothing about nothing...sorry