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Article ; Online: Extracellular Fe

Chankamngoen, Wasutorn / Krungchanuchat, Saowalak / Thongbunchoo, Jirawan / Sirinonthanawech, Naraporn / Teerapornpuntakit, Jarinthorn / Panupinthu, Nattapon / Charoenphandhu, Narattaphol

Scientific reports

2023 Volume 13, Issue 1, Page(s) 21173

Abstract: Iron overload negatively affects bone mass and strength. However, the impact of iron excess on osteocytes-important bone cells for mechanotransduction and remodeling-is poorly understood. Herein, we examined the effects of iron exposure on osteocytes ... ...

Abstract	Iron overload negatively affects bone mass and strength. However, the impact of iron excess on osteocytes-important bone cells for mechanotransduction and remodeling-is poorly understood. Herein, we examined the effects of iron exposure on osteocytes during their maturation process. We discovered that iron overload caused apoptosis of osteocytes in early and late stages of differentiation. Notably, the expression of key proteins for iron entry was downregulated during differentiation, suggesting that mature osteocytes were less susceptible to iron toxicity due to limited iron uptake. Furthermore, iron overload also enriched a subpopulation of mature osteocytes, as indicated by increased expression of Dmp1, a gene encoding protein for bone mineralization. These iron-exposed osteocytes expressed high levels of Sost, Tnfsf11 and Fgf23 transcripts. Consistently, we demonstrated that exogenous FGF23 stimulated the formation and survival of osteoclasts, suggesting its regulatory role in bone resorption. In addition, iron overload downregulated the expression of Cx43, a gene encoding gap junction protein in the dendritic processes, and impaired YAP1 nuclear translocation in response to fluid flow in differentiated osteocytes. It can be concluded that iron overload induces cellular adaptation in differentiating osteocytes, resulting in insensitivity to mechanical stimulation and potential disruption of the balance in bone remodeling.
MeSH term(s)	Humans ; Osteocytes/metabolism ; Mechanotransduction, Cellular/physiology ; Bone Resorption/genetics ; Bone Resorption/metabolism ; Iron/metabolism ; Iron Overload/metabolism ; Adaptor Proteins, Signal Transducing/metabolism
Chemical Substances	Iron (E1UOL152H7) ; SOST protein, human ; Adaptor Proteins, Signal Transducing
Language	English
Publishing date	2023-12-01
Publishing country	England
Document type	Journal Article
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-023-48436-3
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Article ; Online: Regulation of the Hippo-YAP Pathway by G-Protein-Coupled Receptor Signaling.

Yu, Fa-Xing / Zhao, Bin / Panupinthu, Nattapon / Jewell, Jenna L / Lian, Ian / Wang, Lloyd H / Zhao, Jiagang / Yuan, Haixin / Tumaneng, Karen / Li, Hairi / Fu, Xiang-Dong / Mills, Gordon B / Guan, Kun-Liang

Cell

2024 Volume 187, Issue 6, Page(s) 1563–1564

Language	English
Publishing date	2024-03-15
Publishing country	United States
Document type	Published Erratum
ZDB-ID	187009-9
ISSN	1097-4172 ; 0092-8674
ISSN (online)	1097-4172
ISSN	0092-8674
DOI	10.1016/j.cell.2024.02.007
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Article ; Online: Fe3+ opposes the 1,25(OH)2D3-induced calcium transport across intestinal epithelium-like Caco-2 monolayer in the presence or absence of ascorbic acid.

Phummisutthigoon, Sukpapohn / Lertsuwan, Kornkamon / Panupinthu, Nattapon / Aeimlapa, Ratchaneevan / Teerapornpuntakit, Jarinthorn / Chankamngoen, Wasutorn / Thongbunchoo, Jirawan / Charoenphandhu, Narattaphol / Wongdee, Kannikar

PloS one

2022 Volume 17, Issue 8, Page(s) e0273267

Abstract: Although iron is an essential element for hemoglobin and cytochrome synthesis, excessive intestinal iron absorption-as seen in dietary iron supplementation and hereditary disease called thalassemia-could interfere with transepithelial transport of ... ...

Abstract	Although iron is an essential element for hemoglobin and cytochrome synthesis, excessive intestinal iron absorption-as seen in dietary iron supplementation and hereditary disease called thalassemia-could interfere with transepithelial transport of calcium across the intestinal mucosa. The underlying cellular mechanism of iron-induced decrease in intestinal calcium absorption remains elusive, but it has been hypothesized that excess iron probably negates the actions of 1,25-dihydroxyvitamin D [1,25(OH)2D3]. Herein, we exposed the 1,25(OH)2D3-treated epithelium-like Caco-2 monolayer to FeCl3 to demonstrate the inhibitory effect of ferric ion on 1,25(OH)2D3-induced transepithelial calcium transport. We found that a 24-h exposure to FeCl3 on the apical side significantly decreased calcium transport, while increasing the transepithelial resistance (TER) in 1,25(OH)2D3-treated monolayer. The inhibitory action of FeCl3 was considered rapid since 60-min exposure was sufficient to block the 1,25(OH)2D3-induced decrease in TER and increase in calcium flux. Interestingly, FeCl3 did not affect the baseline calcium transport in the absence of 1,25(OH)2D3 treatment. Furthermore, although ascorbic acid is often administered to maximize calcium solubility and to enhance intestinal calcium absorption, it apparently had no effect on calcium transport across the FeCl3- and 1,25(OH)2D3-treated Caco-2 monolayer. In conclusion, apical exposure to ferric ion appeared to negate the 1,25(OH)2D3-stimulated calcium transport across the intestinal epithelium. The present finding has, therefore, provided important information for development of calcium and iron supplement products and treatment protocol for specific groups of individuals, such as thalassemia patients and pregnant women.
MeSH term(s)	Ascorbic Acid/metabolism ; Ascorbic Acid/pharmacology ; Caco-2 Cells ; Calcitriol/metabolism ; Calcitriol/pharmacology ; Calcium/metabolism ; Calcium, Dietary/metabolism ; Electrolytes/metabolism ; Female ; Humans ; Intestinal Absorption ; Intestinal Mucosa/metabolism ; Iron/metabolism ; Iron, Dietary/metabolism ; Pregnancy
Chemical Substances	Calcium, Dietary ; Electrolytes ; Iron, Dietary ; Iron (E1UOL152H7) ; Calcitriol (FXC9231JVH) ; Ascorbic Acid (PQ6CK8PD0R) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-08-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2267670-3
ISSN	1932-6203 ; 1932-6203
ISSN (online)	1932-6203
ISSN	1932-6203
DOI	10.1371/journal.pone.0273267
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Article ; Online: Tissue-specific expression of senescence biomarkers in spontaneously hypertensive rats: evidence of premature aging in hypertension.

Somsura, Ratthapon / Kamkajon, Kanokwan / Chaimongkolnukul, Khuanjit / Chantip, Surachai / Teerapornpuntakit, Jarinthorn / Wongdee, Kannikar / Kamonsutthipaijit, Nuntaporn / Tangtrongsup, Suwimol / Panupinthu, Nattapon / Tiyasatkulkovit, Wacharaporn / Charoenphandhu, Narattaphol

PeerJ

2023 Volume 11, Page(s) e16300

Abstract: Background: Cellular senescence is an age-related physiological process that contributes to tissue dysfunction and accelerated onset of chronic metabolic diseases including hypertension. Indeed, elevation of blood pressure in hypertension coincides with ...

Abstract	Background: Cellular senescence is an age-related physiological process that contributes to tissue dysfunction and accelerated onset of chronic metabolic diseases including hypertension. Indeed, elevation of blood pressure in hypertension coincides with premature vascular aging and dysfunction. In addition, onsets of metabolic disturbance and osteopenia in patients with hypertension have also been reported. It is possible that hypertension enhances premature aging and causes progressive loss of function in multiple organs. However, the landscape of cellular senescence in critical tissues affected by hypertension remains elusive. Materials and methods: Heart, liver, bone, hypothalamus, and kidney were collected from spontaneously hypertensive rats (SHR) and age- and sex-matched normotensive Wistar rats (WT) at 6, 12, 24 and 36 weeks of age ( Results: Real-time PCR revealed that transcript levels of genes encoding CDKIs and SASPs in the heart and liver were upregulated in SHR from 6 to 36 weeks of age. Expression of Conclusion: Premature aging was identified in an organ directly affected by high blood pressure (
MeSH term(s)	Humans ; Rats ; Animals ; Rats, Inbred SHR ; Aging, Premature/genetics ; Interleukin-6/genetics ; Scattering, Small Angle ; Rats, Wistar ; X-Ray Diffraction ; Hypertension/genetics ; Biomarkers ; RNA, Messenger/genetics ; Collagen/therapeutic use
Chemical Substances	Interleukin-6 ; Biomarkers ; RNA, Messenger ; Collagen (9007-34-5)
Language	English
Publishing date	2023-10-19
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2703241-3
ISSN	2167-8359 ; 2167-8359
ISSN (online)	2167-8359
ISSN	2167-8359
DOI	10.7717/peerj.16300
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Article ; Online: CFTR-mediated anion secretion in parathyroid hormone-treated Caco-2 cells is associated with PKA and PI3K phosphorylation but not intracellular pH changes or Na

Chaimana, Rattana / Teerapornpuntakit, Jarinthorn / Jantarajit, Walailak / Lertsuwan, Kornkamon / Krungchanuchat, Saowalak / Panupinthu, Nattapon / Krishnamra, Nateetip / Charoenphandhu, Narattaphol

Biochemistry and biophysics reports

2021 Volume 27, Page(s) 101054

Abstract: Parathyroid hormone (PTH) has previously been shown to enhance the transepithelial secretion of ... ...

Abstract	Parathyroid hormone (PTH) has previously been shown to enhance the transepithelial secretion of Cl
Language	English
Publishing date	2021-06-16
Publishing country	Netherlands
Document type	Journal Article
ZDB-ID	2831046-9
ISSN	2405-5808 ; 2405-5808
ISSN (online)	2405-5808
ISSN	2405-5808
DOI	10.1016/j.bbrep.2021.101054
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Article ; Online: Excessive salt consumption causes systemic calcium mishandling and worsens microarchitecture and strength of long bones in rats.

Tiyasatkulkovit, Wacharaporn / Aksornthong, Sirion / Adulyaritthikul, Punyanuch / Upanan, Pornpailin / Wongdee, Kannikar / Aeimlapa, Ratchaneevan / Teerapornpuntakit, Jarinthorn / Rojviriya, Catleya / Panupinthu, Nattapon / Charoenphandhu, Narattaphol

Scientific reports

2021 Volume 11, Issue 1, Page(s) 1850

Abstract: Excessive salt intake has been associated with the development of non-communicable diseases, including hypertension with several cardiovascular consequences. Although the detrimental effects of high salt on the skeleton have been reported, longitudinal ... ...

Abstract	Excessive salt intake has been associated with the development of non-communicable diseases, including hypertension with several cardiovascular consequences. Although the detrimental effects of high salt on the skeleton have been reported, longitudinal assessment of calcium balance together with changes in bone microarchitecture and strength under salt loading has not been fully demonstrated. To address these unanswered issues, male Sprague-Dawley rats were fed normal salt diet (NSD; 0.8% NaCl) or high salt diet (HSD; 8% NaCl) for 5 months. Elevation of blood pressure, cardiac hypertrophy and glomerular deterioration were observed in HSD, thus validating the model. The balance studies were performed to monitor calcium input and output upon HSD challenge. The HSD-induced increase in calcium losses in urine and feces together with reduced fractional calcium absorption led to a decrease in calcium retention. With these calcium imbalances, we therefore examined microstructural changes of long bones of the hind limbs. Using the synchrotron radiation x-ray tomographic microscopy, we showed that trabecular structure of tibia and femur of HSD displayed a marked increase in porosity. Consistently, the volumetric micro-computed tomography also demonstrated a significant decrease in trabecular bone mineral density with expansion of endosteal perimeter in the tibia. Interestingly, bone histomorphometric analyses indicated that salt loading caused an increase in osteoclast number together with decreases in osteoblast number and osteoid volume. This uncoupling process of bone remodeling in HSD might underlie an accelerated bone loss and bone structural changes. In conclusion, long-term excessive salt consumption leads to impairment of skeletal mass and integrity possibly through negative calcium balance.
MeSH term(s)	Alkaline Phosphatase/genetics ; Alkaline Phosphatase/metabolism ; Animals ; Blood Pressure/drug effects ; Bone Density ; Bone Remodeling/drug effects ; Calcium/blood ; Calcium/metabolism ; Core Binding Factor Alpha 1 Subunit/genetics ; Core Binding Factor Alpha 1 Subunit/metabolism ; Femur/diagnostic imaging ; Femur/drug effects ; Femur/physiopathology ; Femur/ultrastructure ; Heart/drug effects ; Kidney/drug effects ; Kidney/metabolism ; Kidney/pathology ; Male ; Myocardium/metabolism ; Myocardium/pathology ; Porosity ; Rats ; Rats, Sprague-Dawley ; Sodium Chloride, Dietary/pharmacology ; Tibia/diagnostic imaging ; Tibia/drug effects ; Tibia/physiopathology ; Tibia/ultrastructure ; X-Ray Microtomography
Chemical Substances	Core Binding Factor Alpha 1 Subunit ; Runx2 protein, rat ; Sodium Chloride, Dietary ; Alkaline Phosphatase (EC 3.1.3.1) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2021-01-20
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-021-81413-2
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Article ; Online: Mild-intensity physical activity prevents cardiac and osseous iron deposition without affecting bone mechanical property or porosity in thalassemic mice.

Charoenphandhu, Narattaphol / Sooksawanwit, Supagarn / Aeimlapa, Ratchaneevan / Thonapan, Natchayaporn / Upanan, Pornpailin / Adulyaritthikul, Punyanuch / Krungchanuchat, Saowalak / Panupinthu, Nattapon / Teerapornpuntakit, Jarinthorn / Rojviriya, Catleya / Lertsuwan, Kornkamon / Svasti, Saovaros / Wongdee, Kannikar

Scientific reports

2022 Volume 12, Issue 1, Page(s) 5959

Abstract: Thalassemia causes anemia, ineffective erythropoiesis, bone loss and iron accumulation in several tissues, e.g., liver, bone and heart, the last of which leads to lethal cardiomyopathy and arrhythmia. Although exercise reportedly improves bone density in ...

Abstract	Thalassemia causes anemia, ineffective erythropoiesis, bone loss and iron accumulation in several tissues, e.g., liver, bone and heart, the last of which leads to lethal cardiomyopathy and arrhythmia. Although exercise reportedly improves bone density in thalassemic mice, exercise performance is compromised and might pose risk of cardiovascular accident in thalassemic patients. Therefore, we sought to explore whether mild-intensity physical activity (MPA) with 30-50% of maximal oxygen consumption was sufficient to benefit the heart and bone. Herein, male hemizygous β-globin knockout (BKO) mice and wild-type littermates were subjected to voluntary wheel running 1 h/day, 5 days/week for 3 months (MPA group) or kept sedentary (SDN; control). As determined by atomic absorption spectroscopy, BKO-MPA mice had less iron accumulation in heart and bone tissues compared with BKO-SDN mice. Meanwhile, the circulating level of fibroblast growth factor-23-a factor known to reduce serum iron and intestinal calcium absorption-was increased early in young BKO-MPA mice. Nevertheless, MPA did not affect duodenal calcium transport or body calcium retention. Although MPA restored the aberrant bone calcium-phosphorus ratio to normal range, it did not change vertebral calcium content or femoral mechanical properties. Microstructural porosity in tibia of BKO-MPA mice remained unaltered as determined by synchrotron radiation X-ray tomographic microscopy. In conclusion, MPA prevents cardiac and bone iron accumulation, which is beneficial to thalassemic patients with limited physical fitness or deteriorated cardiac performance. However, in contrast to moderate-intensity exercise, MPA does not improve bone mechanical properties or reduce bone porosity.
MeSH term(s)	Animals ; Bone and Bones/diagnostic imaging ; Calcium ; Humans ; Iron ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Motor Activity ; Porosity ; beta-Thalassemia
Chemical Substances	Iron (E1UOL152H7) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-04-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-022-09997-x
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Article ; Online: Prolonged exposure to 1,25(OH)

Rodrat, Mayuree / Wongdee, Kannikar / Panupinthu, Nattapon / Thongbunchoo, Jirawan / Teerapornpuntakit, Jarinthorn / Krishnamra, Nateetip / Charoenphandhu, Narattaphol

Archives of biochemistry and biophysics

2018 Volume 640, Page(s) 10–16

Abstract: Overdose of oral calcium supplement and excessive intestinal calcium absorption can contribute pathophysiological conditions, e.g., nephrolithiasis, vascular calcification, dementia, and cardiovascular accident. Since our previous investigation has ... ...

Abstract	Overdose of oral calcium supplement and excessive intestinal calcium absorption can contribute pathophysiological conditions, e.g., nephrolithiasis, vascular calcification, dementia, and cardiovascular accident. Since our previous investigation has indicated that fibroblast growth factor (FGF)-23 could abolish the 1,25-dihydroxyvitamin D
MeSH term(s)	Caco-2 Cells ; Calcitriol/metabolism ; Calcium/metabolism ; Fibroblast Growth Factors/biosynthesis ; Humans ; Intestinal Absorption ; Intestinal Mucosa/metabolism ; Ion Transport ; Receptors, Calcium-Sensing/metabolism
Chemical Substances	Receptors, Calcium-Sensing ; fibroblast growth factor 23 ; Fibroblast Growth Factors (62031-54-3) ; Calcitriol (FXC9231JVH) ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2018--15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	523-x
ISSN	1096-0384 ; 0003-9861
ISSN (online)	1096-0384
ISSN	0003-9861
DOI	10.1016/j.abb.2017.12.022
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Article ; Online: Tissue-specific expression of senescence biomarkers in spontaneously hypertensive rats

Ratthapon Somsura / Kanokwan Kamkajon / Khuanjit Chaimongkolnukul / Surachai Chantip / Jarinthorn Teerapornpuntakit / Kannikar Wongdee / Nuntaporn Kamonsutthipaijit / Suwimol Tangtrongsup / Nattapon Panupinthu / Wacharaporn Tiyasatkulkovit / Narattaphol Charoenphandhu

PeerJ, Vol 11, p e

evidence of premature aging in hypertension

2023 Volume 16300

Abstract: ... SHR) and age- and sex-matched normotensive Wistar rats (WT) at 6, 12, 24 and 36 weeks of age (n = 10 ...

Abstract	Background Cellular senescence is an age-related physiological process that contributes to tissue dysfunction and accelerated onset of chronic metabolic diseases including hypertension. Indeed, elevation of blood pressure in hypertension coincides with premature vascular aging and dysfunction. In addition, onsets of metabolic disturbance and osteopenia in patients with hypertension have also been reported. It is possible that hypertension enhances premature aging and causes progressive loss of function in multiple organs. However, the landscape of cellular senescence in critical tissues affected by hypertension remains elusive. Materials and Methods Heart, liver, bone, hypothalamus, and kidney were collected from spontaneously hypertensive rats (SHR) and age- and sex-matched normotensive Wistar rats (WT) at 6, 12, 24 and 36 weeks of age (n = 10 animals/group). Changes in mRNA levels of senescence biomarkers namely cyclin-dependent kinase (CDK) inhibitors (CDKIs), i.e., Cdkn2a (encoding p16Ink4a) and Cdkn1a (encoding p21cip1) as well as senescence-associated secretory phenotypes (SASPs), i.e., Timp1, Mmp12, Il6 and Cxcl1, were determined. Additionally, bone collagen alignment and hydroxy apatite crystal dimensions were determined by synchrotron radiation small- and wide-angle X-ray scattering (SAXS/WAXS) techniques. Results Real-time PCR revealed that transcript levels of genes encoding CDKIs and SASPs in the heart and liver were upregulated in SHR from 6 to 36 weeks of age. Expression of Timp1 and Cxcl1 was increased in bone tissues isolated from 36-week-old SHR. In contrast, we found that expression levels of Timp1 and Il6 mRNA were decreased in hypothalamus and kidney of SHR in all age groups. Simultaneous SAXS/WAXS analysis also revealed misalignment of bone collagen fibers in SHR as compared to WT. Conclusion Premature aging was identified in an organ directly affected by high blood pressure (i.e., heart) and those with known functional defects in SHR (i.e., liver and bone). Cellular senescence was not ...
Keywords	Hypertension ; Cellular senescence ; Cyclin-dependent kinase inhibitor (CDKI) ; Senescence-associated secretory phenotype (SASP) ; Spontaneously hypertensive rat (SHR) ; Medicine ; R ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2023-10-01T00:00:00Z
Publisher	PeerJ Inc.
Document type	Article ; Online
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Article ; Online: Impairment of bone microstructure and upregulation of osteoclastogenic markers in spontaneously hypertensive rats.

Tiyasatkulkovit, Wacharaporn / Promruk, Worachet / Rojviriya, Catleya / Pakawanit, Phakkhananan / Chaimongkolnukul, Khuanjit / Kengkoom, Kanchana / Teerapornpuntakit, Jarinthorn / Panupinthu, Nattapon / Charoenphandhu, Narattaphol

Scientific reports

2019 Volume 9, Issue 1, Page(s) 12293

Abstract: Hypertension and osteoporosis are the major non-communicable diseases in the elderly worldwide. Although clinical studies reported that hypertensive patients experienced significant bone loss and likelihood of fracture, the causal relationship between ... ...

Abstract	Hypertension and osteoporosis are the major non-communicable diseases in the elderly worldwide. Although clinical studies reported that hypertensive patients experienced significant bone loss and likelihood of fracture, the causal relationship between hypertension and osteoporosis has been elusive due to other confounding factors associated with these diseases. In this study, spontaneously hypertensive rats (SHR) were used to address this relationship and further explored the biophysical properties and the underlying mechanisms. Long bones of the hind limbs from 18-week-old female SHR were subjected to determination of bone mineral density (BMD) and their mechanical properties. Using synchrotron radiation X-ray tomographic microscopy (SRXTM), femoral heads of SHR displayed marked increase in porosity within trabecular area together with decrease in cortical thickness. The volumetric micro-computed tomography also demonstrated significant decreases in trabecular BMD, cortical thickness and total cross-sectional area of the long bones. These changes also led to susceptibility of the long bones to fracture indicated by marked decreases in yield load, stiffness and maximum load using three-point bending tests. At the cellular mechanism, an increase in the expression of osteoclastogenic markers with decrease in the expression of alkaline phosphatase was found in primary osteoblast-enriched cultures isolated from long bones of these SHR suggesting an imbalance in bone remodeling. Taken together, defective bone mass and strength in hypertensive rats were likely due to excessive bone resorption. Development of novel therapeutic interventions that concomitantly target hypertension and osteoporosis should be helpful in reduction of unwanted outcomes, such as bone fractures, in elderly patients.
MeSH term(s)	Animals ; Biomarkers/metabolism ; Blood Pressure ; Bone Density ; Bone and Bones/anatomy & histology ; Bone and Bones/diagnostic imaging ; Cell Shape ; Diastole/physiology ; Female ; Femur/anatomy & histology ; Femur/diagnostic imaging ; Gene Expression Regulation ; Organ Size ; Osteoblasts/metabolism ; Osteogenesis ; RNA, Messenger/genetics ; RNA, Messenger/metabolism ; Rats, Inbred SHR ; Systole/physiology ; Tibia/anatomy & histology ; Tibia/diagnostic imaging ; Up-Regulation ; X-Ray Microtomography
Chemical Substances	Biomarkers ; RNA, Messenger
Language	English
Publishing date	2019-08-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-019-48797-8
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