Biology subjects

Okoshi, K.

Publications and source records attributed to Okoshi, K..

3 recordsLinked to original sources

bioRxiv2026

Secretory ferritins mediate iron delivery during magnetite tooth formation in chitons

Iron is essential to most organisms, yet unbound iron is toxic, necessitating tight regulation of its storage and transport. Chitons concentrate extraordinary amounts of iron in radular tissue to form magnetite-mineralized teeth, but how iron is supplied to developing teeth remains unclear. Here, synchrotron radiation X-ray fluorescence mapping resolved the spatiotemporal redistribution of iron from the radular epithelium toward developing teeth. Integrated transcriptomic and proteomic analyses identified secretory ferritin subunits in radular tissue whose genes were highly expressed in the midgut gland and whose proteins were also present in the hemolymph. In vivo fluorescence tracking showed that circulating ferritin was selectively taken up by the radular epithelium, and following injection of Ag-loaded hemolymph ferritin, Ag was detected in developing teeth. Together, these findings support a model in which secretory ferritins produced in the midgut gland transport iron through the hemolymph to the radula, enabling the pronounced iron accumulation required for tooth mineralization.

molecular biology↗

bioRxiv2024

Radular teeth matrix protein 1 directs iron oxide deposition in chiton teeth

Chitons deposit magnetite, a type of iron oxide, on the cusps of their radular teeth. The molecules that control the deposition of iron oxide on chiton teeth have not been identified. Using immunofluorescence staining, we found that chiton-specific radular teeth matrix protein 1 (RTMP1) is highly expressed in tooth epithelial cells prior to iron oxide deposition and preexists in the cusp at the site of iron oxide deposition. RTMP1 was found to be secreted from the elongated epithelial cells covering teeth and transported into teeth through microvilli. Moreover, recombinant RTMP1 exhibited the ability to form iron oxide. These results indicate that RTMP1 is a key molecule for iron oxide deposition in chiton teeth.

molecular biology↗

bioRxiv2020

Preventive training interferes with mRNA-encoding myosin 7 and collagen I expression during pulmonary arterial hypertension

To gain insight on the impact of preventive exercise during pulmonary arterial hypertension (PAH), we evaluated the gene expression of myosins and gene-encoding proteins associated with the extracellular matrix remodeling of right hypertrophied ventricles. We used 32 male Wistar rats, separated in four groups: Sedentary Control (S; n=8); Control with Training (T; n=8); Sedentary with Pulmonary Arterial Hypertension (SPAH; n=8); and Pulmonary Arterial Hypertension with Training (TPAH; n=8). The rats trained for thirteen weeks on a treadmill. They had two weeks of adaptation training. The PAH was induced by application of monocrotaline 60 mg/kg. Consequential right ventricular dysfunction was observed after the 10th week of training. Rats in the control group received saline application. At the end of the 13th week, echocardiography analysis confirmed cardiac dysfunction. Collagen content and organization was assessed through picrosirius red staining and fractal dimension (FD) analysis, respectively. Transcript abundance was estimated through reverse transcription-quantitative PCR (RT-qPCR). Cardiac dysfunction was confirmed by the reduction in maximum pulmonary artery velocity and pulmonary artery acceleration time. Through histomorphometric assessment, we found no differences in the interstitial collagen FD between groups. Regarding gene expression, myh7 gene expression was upregulated in the TPAH group. However, this did not occur with the S group. PAH also increased the mRNA abundance of col1a1 in the SPAH and TPAH groups. Moreover, the TPAH group showed a higher abundance of this gene when compared to the S group. With these findings, we concluded that preventive exercise had a positive impact on compensated hypertrophy during pulmonary hypertension. This can be explained in part by the modulation of the extracellular matrix and myosin gene expression in trained rats.

molecular biology↗