The Anatomical Record : Advances in Integrative Anatomy and Evolutionary Biology

doi: 10.1002/ar.1092290101pmid: N/A

Diaz‐Flores, Lucio; Gutierrez, Ricardo; Gonzalez, Pilar; Varela, Hilda

doi: 10.1002/ar.1092290102pmid: 1996774

Autogeneic perichondrium was implanted above the cremaster muscle of the rat, and the new formation of two types of cartilage (types I and II) was confirmed. Also, granulation tissue was observed before the type II cartilage formation. Under these conditions, the contribution to the neocartilage of graft bed derived cells, mainly of the venule pericytes, was studied. To follow the pericyte lineage, we used a marker—Monastral Blue B—the administration of which was based on the principle of vascular labeling. While the perichondrium was kept free, before its implantation, the preformed (preexisting) venules in the cremaster muscle were exclusively labeled with Monastral Blue B, which was incorporated into the cytoplasm of pericytes and endothelial cells. After perichondrium implantation, the following sequence in tracer distribution was demonstrated. During the earlier stages, labeling was restricted to the pericytes and endothelial cells of venules in the graft bed. Later the tracer was observed in some endothelial cells and pericytes of the growing vessels and in fibroblast‐like cells of the granulation tissue. Finally, some type II neochondrocytes appeared labeled. Tracer was not found in type I neochondrocytes. The presence of label in type II neochondrocytes demonstrates that they arise from progenitor cells present in the graft bed, principally from small venule pericytes. Therefore, the findings in this study provide greater evidence that surrounding soft tissues may increase the process of cartilage regeneration from cells present in the perichondrium by contributing inducible perivascular cells.

Amano, Osamu; Kataoka, Seiki; Yamamoto, Toshi Yuki

doi: 10.1002/ar.1092290103pmid: 1996788

Asymmetric thick unit membranes were observed on the luminal surface, fusiform vesicles, and multivesicular bodies of superficial cells of rat transitional epithelium. When HRP‐labeled Ricinus communis lectin (RCA‐I) was injected into the rat urinary bladder, RCA‐I was deposited along the luminal cell membrane and in some multivesicular bodies, but not in the fusiform vesicles either before or after contraction. When the bladder was sliced by Vibratome and stained with HRP‐labeled RCA‐I after fixation, RCA‐I was observed in many cell organelles, including fusiform vesicles and multivesicular bodies as well as the luminal surface. When small pieces of tissue were stained en‐bloc with HRP‐labeled RCA‐I, RCA‐I was found along the luminal cell surface but not in the fusiform vesicles nor the multivesicular bodies. When HRP alone was injected into the bladder, HRP was observed in some multivesicular bodies after contraction but not in the fusiform vesicles. Various lysosomes were observed by electron microscopy. Some were wrapping multivesicular bodies in ringlike fashion, and some contained asymmetric unit membranes. These findings suggest that the asymmetric unit membranes are carried to the luminal cell membrane via the fusiform vesicles and that old luminal cell membranes are removed via the multivesicular bodies to be degraded by lysosomes.

Suarez‐Quian, Carlos A.; An, Qu; Jelesoff, Nicole; Dym, Martin

doi: 10.1002/ar.1092290104pmid: 1996781

A morphological and immunocytochemical study of the Golgi apparatus in pachytene spermatocytes was performed in an effort to correlate the structure and function of this organelle during meiotic prophase. In stages I‐III of the cycle, the Golgi complex of pachytene spermatocytes is a flattened discoid, 0.5–1 μm in diameter, composed of vesicles interspersed with classically described Golgi cisternae. During subsequent maturation of pachytene spermatocytes (stages IV–XIII), the size of the Golgi complex increases significantly, attaining a size of 2–3 μm. However, unlike pachytene spermatocytes of stages I–III, the majority of the Golgi complex of more mature spermatocytes is characterized by an abundance of distinct stacks of cisternae interspersed with numerous vesicles and tubules. The composition of the Golgi complex was also studied by using two monoclonal antibodies that recognize either the cis or the trans Golgi cisternae, respectively, and employing biotin‐streptavidin‐peroxidase immunocytochemistry in 5 μm frozen sections of testes. Immunodetection of the distinct cisternae revealed that the increase in size of the Golgi complex during maturation of pachytene spermatocytes was due predominantly to an accumulation of trans Golgi; the amount of cis Golgi remained unchanged.

Van Nassauw, Luc; Callebaut, Marc

doi: 10.1002/ar.1092290105pmid: 1996782

In the present study, we searched for the presence of granulosa lipid spheres, of lacunae, and of the smooth‐muscle markers desmin and α‐smooth‐muscle actin, in the wall of the POF1 of the quail ovary. Lacunae, using the labelled yolk technique, were visible as large cavities in the POF1 wall. The immunohistochemical localization of desmin was similar to that observed in preovulatory follicles. A similar distribution was observed using an anti‐α‐smooth‐muscle actin antiserum, but the cells of the theca externa were also positively stained. The general conclusion was that the studied structures were similarly localized in the follicle wall, before and during the day after ovulation, but that they are more obvious in the POF, due to its general contracted state.

Hermo, L.; Oko, R.; Hecht, N. B.

doi: 10.1002/ar.1092290106pmid: 1996783

The cells of the seminiferous epithelium of the rat testis are a rich source of microtubules and contain distinct microtubular structures such as the meiotic spindle and manchette. Microtubule diversity can be maintained by differential genetic expression of the multiple α‐ and β‐tubulin polypeptides or by tubulin monomer acetylation and detyrosination, post‐translational modifications of α‐tubulin. In the present analysis, antibodies that specifically recognize acetylated (antiacetylated), tyrosinated (anti‐Tyr) and detyrosinated (anti‐Glu) α‐tubulins were employed to examine the distribution of post‐translationally modified microtubules in the cells of the seminiferous epithelium.

Iseki, Shoichi; Kanda, Tatsuo; Hitomi, Masahiro; Ono, Teruo

doi: 10.1002/ar.1092290107pmid: 1996784

With the use of specific antibodies against three structurally different fatty acid binding proteins (FABPs), viz, liver FABP (L‐FABP), heart FABP (H‐FABP), and intestinal FABP (I‐FABP), the localization and relative amount of the immunoreactive proteins were determined by immunoblotting and immunocytochemistry in the gastric epithelium of rats during prenatal and postnatal development. H‐FABP immunoreactivity was first detected at embryonic day 20 (E20), with predominant localization in the parietal cells, whereas I‐FABP immunoreactivity was detected at the day of birth in the surface mucous cells. Both immunoreactivities were continuously localized in the same cell types with increasing intensity into adulthood. In contrast, the immunoreactivity for L‐FABP showed remarkable changes in intensity and localization during development of the rat stomach. It was first detected in the surface mucous cells of E19. In the first 2 weeks of postnatal life, i.e., the suckling period, L‐FABP immunoreactivity reached a peak in intensity and was localized not only in the surface mucous cells, but also in some of the parietal cells, brush cells, and endocrine D cells. In the following few weeks of weaning, the reactivity of surface mucous cells and parietal cells disappeared, leaving only a small amount of total L‐FABP immunoreactivity in the adult stomach, which was localized exclusively in the brush cells and D cells. These results revealed that the appearance of the three types of FABPs in the rat stomach is specific to cell types and developmental stages.

Cooney, Rodger A.; Chopra, Dharam P.

doi: 10.1002/ar.1092290108pmid: 1996785

Limited studies have described the ultrastructure of trachea of late fetal and neonatal hamsters but the effects of parturition and the onset of breathing on structure have not been discussed. This study describes morphological features of ante‐ and post‐partum tracheal mucosa and submucosa and contrasts these features in fetal and neonatal hamster siblings. Significant differences between these siblings are noted in tracheal cells interfacing the lumen. Such cells of the fetal animals usually possessed cytoplasm of medium electron density with cisternal rough endoplasmic reticulum (RER). Surface membranes of these cells possessed numerous microvilli. In contrast, corresponding cells of post‐natal animals often had lucent cytoplasm with mostly tubular or vesicular RER. Surface membranes of these cells possessed microplicae (microridges).

Snyder, Jeanne M.; Magliato, Susan A.

doi: 10.1002/ar.1092290109pmid: 1996786

Rabbit lung type II cell differentiation was evaluated by use of ultrastructural, morphometric techniques. Fetal lung epithelial cells decreased in size dramatically from day 19 to day 21 of gestation. Thereafter, the cell and cytoplasmic cross‐sectional area declined gradually until the neonatal time point. The tall columnar cell shape characteristic of fetal lung epithelial cells at early stages of development became cuboidal by day 24 of gestation. The number of mitochondria per μm2 cytoplasmic area in presumptive alveolar epithelial cells and the mitochondrial volume density increased toward the end of gestation. The volume density of glycogen pools within fetal lung epithelial cells reached a plateau on day 21 of gestation and then declined sharply on day 26 of gestation in lamellar body‐containing, type II epithelial cells. Lamellar bodies increased in number and volume density in epithelial cells starting on day 26 of gestation and peaked with respect to these parameters in the neonatal lung tissue. Multivesicular bodies, which are thought to be a precursor to the lamellar body, became more prominent in differentiated type II cells on day 26 of gestation and increased in volume density from day 28 of gestation to the adult time point. The distance between mesenchymal and epithelial cells in fetal lung tissue declined sharply between days 24 and 26 of gestation but remained relatively constant thereafter. Foot processes extending from connective tissue cells contiguous to the epithelium were generally more numerous than those extending from the basal plasma membrane of epithelial cells at every stage of development examined. These data quantitate for the first time key ultrastructural events that occur during the differentiation of fetal lung epithelial cells in vivo.

Kang, Yuan‐Hsu; Williams, Robert

doi: 10.1002/ar.1092290110pmid: 1996787

Endotoxin (lipopolysaccharide, LPS) induces endothelial injury in arterial vessels. Fibronectin is known to be involved in cell attachment and wound repair. The present study was designed to elucidate the effect of LPS on the production and distribution of fibronectin in relation to injury and repair in rat aortic endothelium. Male Sprague‐Dawley rats were sacrificed for ultrastructural and immunocytochemical evaluations at 1, 3, 6, 24, and 48 hr after a single intravenous injection of 1.5 or 3 mg/kg body weight E. coli LPS. Apparent morphological signs of endothelial injury, including cell detachment, denudation, cell death, and edema were observed 1–48 hr after injection. Parietal thrombosis and leukocyte diapedesis were also observed in the aorta. A profound increase in subendothelial fibronectin was found following LPS treatment. However, no distinct change in intracellular fibronectin was observed in the same endothelium until 24 hr after injection. Using horseradish peroxidase (HRP) and anti‐fibronectin‐HRP antibody as tracers, LPS was also found to increase permeability and extravasation of plasma proteins (fibronectin) of the aortic endothelium. The increase of subendothelial fibronectin possibly resulted from increased influx and sequestration of plasma fibronectin. This increase may provide a firm substratum for reendothelialization after vascular injury.