The Golgi apparatus is known to underpin many important cellular homeostatic functions, including trafficking, sorting and modifications of proteins or lipids. These functions are dysregulated in neurodegenerative diseases, cancer, infectious diseases and cardiovascular diseases, and the number of disease‑related genes associated with Golgi apparatus is on the increase. Recently, many studies have suggested that the mutations in the genes encoding Golgi resident proteins can trigger the occurrence of diseases. By summarizing the pathogenesis of these genetic diseases, it was found that most of these diseases have defects in membrane trafficking. Such defects typically result in mislocalization of proteins, impaired glycosylation of proteins, and the accumulation of undegraded proteins. In the present review, we aim to understand the patterns of mutations in the genes encoding Golgi resident proteins and decipher the interplay between Golgi resident proteins and membrane trafficking pathway in cells. Furthermore, the detection of Golgi resident protein in human serum samples has the potential to be used as a diagnostic tool for diseases, and its central role in membrane trafficking pathways provides possible targets for disease therapy. Thus, we also introduced the clinical value of Golgi apparatus in the present review.

/pdf/the-role-of-the-golgi-apparatus-in-disease-review-apynzok9v3.pdf

The role of the Golgi apparatus in disease (Review).

The ultrastructure of myocardial cells was studied in four patients with left ventricular myocardial hypertrophy due to aortic and/or mitral valvular disease. Signs of cellular lysis and synthesis were present in juxtanuclear, interfibrillar, and subsarcolemmal areas. Subsarcolemmal areas contained a granular matrix with foci of polyribosomes, mitochondria, well preserved membranes, a proliferating sarcoplasmic reticulum, and thick and thin filaments and Z-band formations at different stages of development. Z-band substance and thin filaments appeared in the cytoplasm in close proximity to free polyribosomes and endoplasmic membranes and were seemingly not associated with the sarcolemma. These findings were interpreted as evidence for a proteosynthetic activity leading to the formation of new myofibrils and sarcomeres during the chronic stage of hypertrophy. Comparative studies showed that this process has much in common with the genesis of contractile cardiac units in the mammalian embryo. Anomalous Z-band accumulations were studied in normal myocardial cells of various vertebrates and in cells of the overloaded human heart. No evidence of a proteosynthetic activity was detected in the expanded Z-bands.

Ultrastructural studies on the growth of filaments and sarcomeres in mechanically overloaded human hearts.

Atrial natriuretic peptide (ANP) is a newly discovered peptide hormone present mainly in the atria. We investigated the occurrence and distribution of ANP immunoreactivity in the myocardiocytes of the ventricles of spontaneously hypertensive rats by use of immunocytochemistry at both light and electron microscopic level. ANP immunoreactivity was found in the specific granules in the cytoplasm of the cardiocytes in the subendocardium and the myocardium of the ventricles, as well as in the atria. The specific granules found in the ventricles of hypertensive rats were similar in size, shape, and ANP immunoreactive content to those in the atria. The abundance of ANP immunoreactivity in the left ventricle is greater than that in the right, and appears to increase with increasing severity of hypertension. Conversely, the overall content of ANP in the atria of hypertensive rats was decreased when compared with that in age-matched normotensive rats. The present findings indicate that ventricles may become a major source for ANP synthesis and release during hypertension, and may play important roles in cardiac endocrine pathology and cardiac hypertrophy.

Light and electron microscopic localization of atrial natriuretic peptide in the heart of spontaneously hypertensive rat.

Cardiac hypothermia evaluated by ultrastructural studies in man.

A close spatial relationship between specific granules containing atrial natriuretic factor (ANF) and microtubules was demonstrated in primary cultures of neonatal rat cardiac myocytes. For the detection of specific granules and microtubules, the myocytes were double immunolabeled with antibodies against alpha-ANF and beta-tubulin and examined by conventional fluorescence or laser scanning confocal microscopy. In addition, the ultrastructural distribution of specific granules was demonstrated by electron microscopy. In the atrial myocytes, ANF was stored in numerous specific granules that were mainly localized in the perinuclear sarcoplasm. In the ventricular myocytes, however, a minority of the cells (10%) exhibited limited ANF immunoreactivity after 4 days in culture. Microtubules were present throughout the sarcoplasm of the myocytes. They were most densely packed in the perinuclear regions. Depolymerization of the microtubules with nocodazole was followed by dispersal of ANF immunostaining both in the atrial myocytes and in the ventricular myocytes exhibiting ANF immunoreactivity. When the microtubules were allowed to recover, the perinuclear distribution of specific granules, as seen in non-treated myocytes, reappeared. Measurements of secreted immunoreactive ANF by radioimmunoassay revealed that the secretion of ANF from atrial myocytes into the medium was significantly reduced following nocodazole treatment, whereas a similar decrease in secretion from ventricular myocytes was not observed. These findings indicate that ANF-containing specific granules are closely associated with microtubules within the myocytes. It is suggested that secretion of ANF from the atrial myocytes, in contrast to the ventricular myocytes, is microtubule-dependent.

Microtubule-associated distribution of specific granules and secretion of atrial natriuretic factor in primary cultures of rat cardiomyocytes.

The electron microscopic aspects of myocardial cells in several types of mechanically overloaded heart are reviewed. Alterations which may be interpreted as degenerative changes are all the more frequent as the load is more severe. They seem to be the cause of the interstitial fibrosis which often accompanies hypertrophy. Their mechanism is dubious: swelling of mitochondria and intracellular lipidosis, which could signify cellular hypoxia, are rarely present. Other changes are characteristic of an increase of proteosynthesis and of the active growth of the main structures of the cell: myofibrils, mitochondria, T- and L-tubules. Some pictures of myofibrillar growth are not always easily distinguished from those of myofibrillar lesions. The mitochondria/myofibril ratio may be modified or not. The apparent volume of the mitochondria may remain normal while their density increases, which implies a decrease of their average size. In severe and long-lasting overloads, hypertrophy and hyperplasia of the Golgi apparatus and multiplication of granules of the auricular type evoke a regression of the cell toward its fetal type.

Cellular changes and damage in mechanically overloaded hearts.

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Cellular changes and damage in mechanically overloaded hearts.