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Willekens, S. M. A., Morini, F., Mediavilla, T., Nilsson, E., Orädd, G., Hahn, M., . . . Marcellino, D. (2024). An MR-based brain template and atlas for optical projection tomography and light sheet fluorescence microscopy in neuroscience. Frontiers in Neuroscience, 18, Article ID 1328815.
Åpne denne publikasjonen i ny fane eller vindu >>An MR-based brain template and atlas for optical projection tomography and light sheet fluorescence microscopy in neuroscience
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2024 (engelsk)Inngår i: Frontiers in Neuroscience, ISSN 1662-4548, E-ISSN 1662-453X, Vol. 18, artikkel-id 1328815Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Introduction: Optical Projection Tomography (OPT) and light sheet fluorescence microscopy (LSFM) are high resolution optical imaging techniques, ideally suited for ex vivo 3D whole mouse brain imaging. Although they exhibit high specificity for their targets, the anatomical detail provided by tissue autofluorescence remains limited.

Methods: T1-weighted images were acquired from 19 BABB or DBE cleared brains to create an MR template using serial longitudinal registration. Afterwards, fluorescent OPT and LSFM images were coregistered/normalized to the MR template to create fusion images.

Results: Volumetric calculations revealed a significant difference between BABB and DBE cleared brains, leading to develop two optimized templates, with associated tissue priors and brain atlas, for BABB (OCUM) and DBE (iOCUM). By creating fusion images, we identified virus infected brain regions, mapped dopamine transporter and translocator protein expression, and traced innervation from the eye along the optic tract to the thalamus and superior colliculus using cholera toxin B. Fusion images allowed for precise anatomical identification of fluorescent signal in the detailed anatomical context provided by MR.

Discussion: The possibility to anatomically map fluorescent signals on magnetic resonance (MR) images, widely used in clinical and preclinical neuroscience, would greatly benefit applications of optical imaging of mouse brain. These specific MR templates for cleared brains enable a broad range of neuroscientific applications integrating 3D optical brain imaging.

sted, utgiver, år, opplag, sider
Frontiers Media S.A., 2024
Emneord
brain template, LSFM, mesoscopic imaging, MRI, neuroimaging, OPT
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-223641 (URN)10.3389/fnins.2024.1328815 (DOI)001198866200001 ()38601090 (PubMedID)2-s2.0-85189910322 (Scopus ID)
Forskningsfinansiär
The Kempe FoundationsSwedish Research Council, 2020-06224Swedish Research Council, 2018-05851Swedish Research Council, 2020-02300Novo Nordisk FoundationFamiljen Erling-Perssons Stiftelse
Tilgjengelig fra: 2024-04-24 Laget: 2024-04-24 Sist oppdatert: 2024-04-24bibliografisk kontrollert
Lehrstrand, J., Davies, W. I. L., Hahn, M., Korsgren, O., Alanentalo, T. & Ahlgren, U. (2024). Illuminating the complete ß-cell mass of the human pancreas - signifying a new view on the islets of Langerhans. Nature Communications, 15(1), Article ID 3318.
Åpne denne publikasjonen i ny fane eller vindu >>Illuminating the complete ß-cell mass of the human pancreas - signifying a new view on the islets of Langerhans
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2024 (engelsk)Inngår i: Nature Communications, E-ISSN 2041-1723, Vol. 15, nr 1, artikkel-id 3318Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Pancreatic islets of Langerhans play a pivotal role in regulating blood glucose homeostasis, but critical information regarding their mass, distribution and composition is lacking within a whole organ context. Here, we apply a 3D imaging pipeline to generate a complete account of the insulin-producing islets throughout the human pancreas at a microscopic resolution and within a maintained spatial 3D context. These data show that human islets are far more heterogenous than previously accounted for with regards to their size distribution and cellular make up. By deep tissue 3D imaging, this in-depth study demonstrates that 50% of the human insulin-expressing islets are virtually devoid of glucagon-producing α-cells, an observation with significant implications for both experimental and clinical research.

sted, utgiver, år, opplag, sider
Springer Nature, 2024
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-223844 (URN)10.1038/s41467-024-47686-7 (DOI)001204844700001 ()38632302 (PubMedID)2-s2.0-85190704494 (Scopus ID)
Forskningsfinansiär
The Kempe Foundations, SMK-1455Swedish Research Council, 2017- 01307Swedish Research Council, 2023-02221Swedish Child Diabetes FoundationNovo Nordisk Foundation, NNF21OC0069771Novo Nordisk Foundation, NNF21OC0084520Novo Nordisk Foundation, NNF20OC0063600Insamlingsstiftelsen Diabetes Wellness, PG21-6566Ernfors Foundation, 2023Diabetesfonden, DIA2021-59
Tilgjengelig fra: 2024-04-29 Laget: 2024-04-29 Sist oppdatert: 2024-04-29bibliografisk kontrollert
Hahn, M. & Ahlgren, U. (2023). 3D optical molecular imaging of the rodent pancreas by OPT and LSFM. In: Anna Moore; Ping Wang (Ed.), Type-1 diabetes: methods and protocols (pp. 1-19). New York: Humana Press
Åpne denne publikasjonen i ny fane eller vindu >>3D optical molecular imaging of the rodent pancreas by OPT and LSFM
2023 (engelsk)Inngår i: Type-1 diabetes: methods and protocols / [ed] Anna Moore; Ping Wang, New York: Humana Press, 2023, , s. 19s. 1-19Kapittel i bok, del av antologi (Fagfellevurdert)
Abstract [en]

The rodent pancreas is the prevalent model system for preclinical diabetes research. However, due to the compound endocrine–exocrine organization of the gland, with the endocrine islets of Langerhans scattered by the thousands throughout the much greater exocrine parenchyma, stereological assessments of endocrine cell mass, commonly insulin-producing ß-cells, are exceedingly challenging. In recent years, optical mesoscopic imaging techniques such as optical projection tomography (OPT) and light sheet fluorescence microscopy (LSFM) have seen dramatic developments, enabling 3D visualization of fluorescently labeled cells in mm- to cm-sized tissues with μm resolution. Here we present a protocol for 3D visualization and “absolute” quantitative assessments of, for example, islet mass throughout the volume of rodent pancreata with maintained spatial context.

sted, utgiver, år, opplag, sider
New York: Humana Press, 2023. s. 19
Serie
Methods in Molecular Biology, ISSN 1064-3745, E-ISSN 1940-6029 ; 2592
Emneord
Diabetes, Insulin, Islets of Langerhans, Light sheet fluorescence microscopy, Optical clearing, Optical projection tomography, Pancreas, Rodents, Whole mount immunohistochemistry
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-202060 (URN)10.1007/978-1-0716-2807-2_1 (DOI)36507982 (PubMedID)2-s2.0-85144475952 (Scopus ID)978-1-0716-2806-5 (ISBN)978-1-0716-2809-6 (ISBN)978-1-0716-2807-2 (ISBN)
Tilgjengelig fra: 2023-01-03 Laget: 2023-01-03 Sist oppdatert: 2023-03-23bibliografisk kontrollert
Chotiwan, N., Rosendal, E., Willekens, S. M. A., Schexnaydre, E., Nilsson, E., Lindquist, R., . . . Överby, A. K. (2023). Type I interferon shapes brain distribution and tropism of tick-borne flavivirus. Nature Communications, 14(1), Article ID 2007.
Åpne denne publikasjonen i ny fane eller vindu >>Type I interferon shapes brain distribution and tropism of tick-borne flavivirus
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2023 (engelsk)Inngår i: Nature Communications, E-ISSN 2041-1723, Vol. 14, nr 1, artikkel-id 2007Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Viral tropism within the brain and the role(s) of vertebrate immune response to neurotropic flaviviruses infection is largely understudied. We combine multimodal imaging (cm-nm scale) with single nuclei RNA-sequencing to study Langat virus in wildtype and interferon alpha/beta receptor knockout (Ifnar-/-) mice to visualize viral pathogenesis and define molecular mechanisms. Whole brain viral infection is imaged by Optical Projection Tomography coregistered to ex vivo MRI. Infection is limited to grey matter of sensory systems in wildtype mice, but extends into white matter, meninges and choroid plexus in Ifnar-/- mice. Cells in wildtype display strong type I and II IFN responses, likely due to Ifnb expressing astrocytes, infiltration of macrophages and Ifng-expressing CD8+ NK cells, whereas in Ifnar-/-, the absence of this response contributes to a shift in cellular tropism towards non-activated resident microglia. Multimodal imaging-transcriptomics exemplifies a powerful way to characterize mechanisms of viral pathogenesis and tropism.

sted, utgiver, år, opplag, sider
Springer Nature, 2023
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-206780 (URN)10.1038/s41467-023-37698-0 (DOI)000967732600009 ()37037810 (PubMedID)2-s2.0-85152115180 (Scopus ID)
Forskningsfinansiär
The Kempe Foundations, SMK-1532Knut and Alice Wallenberg Foundation, KAW2015.0284Swedish Research Council, 2018-05851Swedish Research Council, 2017-01307Swedish Research Council, 2020-06224Swedish Research Council, 2021-06602
Tilgjengelig fra: 2023-04-24 Laget: 2023-04-24 Sist oppdatert: 2023-09-05bibliografisk kontrollert
Hahn, M., Nord, C., van Krieken, P. P., Berggren, P.-O., Ilegems, E., Cheddad, A. & Ahlgren, U. (2022). Quantitative 3D OPT and LSFM datasets of pancreata from mice with streptozotocin-induced diabetes. Scientific Data, 9, Article ID 558.
Åpne denne publikasjonen i ny fane eller vindu >>Quantitative 3D OPT and LSFM datasets of pancreata from mice with streptozotocin-induced diabetes
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2022 (engelsk)Inngår i: Scientific Data, E-ISSN 2052-4463, Vol. 9, artikkel-id 558Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Mouse models for streptozotocin (STZ) induced diabetes probably represent the most widely used systems for preclinical diabetes research, owing to the compound’s toxic effect on pancreatic β-cells. However, a comprehensive view of pancreatic β-cell mass distribution subject to STZ administration is lacking. Previous assessments have largely relied on the extrapolation of stereological sections, which provide limited 3D-spatial and quantitative information. This data descriptor presents multiple ex vivo tomographic optical image datasets of the full β-cell mass distribution in mice subject to single high and multiple low doses of STZ administration, and in glycaemia recovered mice. The data further include information about structural features, such as individual islet β-cell volumes, spatial coordinates, and shape as well as signal intensities for both insulin and GLUT2. Together, they provide the most comprehensive anatomical record of the effects of STZ administration on the islet of Langerhans in mice. As such, this data descriptor may serve as reference material to facilitate the planning, use and (re)interpretation of this widely used disease model.

sted, utgiver, år, opplag, sider
Nature Publishing Group, 2022
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-193538 (URN)10.1038/s41597-022-01546-5 (DOI)000852384000002 ()36088402 (PubMedID)2-s2.0-85138129001 (Scopus ID)
Forskningsfinansiär
Swedish Diabetes AssociationUmeå UniversityFamiljen Erling-Perssons StiftelseEU, FP7, Seventh Framework Programme, 289932EU, FP7, Seventh Framework Programme, 613879Knut and Alice Wallenberg FoundationSwedish Research CouncilNovo Nordisk
Merknad

Originally included in thesis in manuscript form.

Tilgjengelig fra: 2022-04-06 Laget: 2022-04-06 Sist oppdatert: 2022-10-03bibliografisk kontrollert
Hahn, M., Nord, C., Eriksson, M., Morini, F., Alanentalo, T., Korsgren, O. & Ahlgren, U. (2021). 3D imaging of human organs with micrometer resolution - applied to the endocrine pancreas. Communications Biology, 4(1), Article ID 1063.
Åpne denne publikasjonen i ny fane eller vindu >>3D imaging of human organs with micrometer resolution - applied to the endocrine pancreas
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2021 (engelsk)Inngår i: Communications Biology, E-ISSN 2399-3642, Vol. 4, nr 1, artikkel-id 1063Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The possibility to quantitatively study specific molecular/cellular features of complete human organs with preserved spatial 3D context would have widespread implications for pre-clinical and clinical medicine. Whereas optical 3D imaging approaches have experienced a formidable revolution, they have remained limited due to current incapacities in obtaining specific labelling within large tissue volumes. We present a simple approach enabling reconstruction of antibody labeled cells within entire human organs with preserved organ context. We demonstrate the utility of the approach by providing volumetric data and 3D distribution of hundreds of thousands of islets of Langerhans within the human pancreas. By assessments of pancreata from non-diabetic and type 2 diabetic individuals, we display previously unrecognized features of the human islet mass distribution and pathology. As such, this method may contribute not only in unraveling new information of the pancreatic anatomy/pathophysiology, but it may be translated to essentially any antibody marker or organ system.

sted, utgiver, år, opplag, sider
Springer Nature, 2021
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-187770 (URN)10.1038/s42003-021-02589-x (DOI)000694906000003 ()2-s2.0-85114856810 (Scopus ID)
Tilgjengelig fra: 2021-09-22 Laget: 2021-09-22 Sist oppdatert: 2023-03-24bibliografisk kontrollert
Davies, W. I. L., Sghari, S., Upton, B. A., Nord, C., Hahn, M., Ahlgren, U., . . . Gunhaga, L. (2021). Distinct opsin 3 (Opn3) expression in the developing nervous system during mammalian embryogenesis. eNeuro, 8(5), Article ID ENEURO.0141-21.2021.
Åpne denne publikasjonen i ny fane eller vindu >>Distinct opsin 3 (Opn3) expression in the developing nervous system during mammalian embryogenesis
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2021 (engelsk)Inngår i: eNeuro, E-ISSN 2373-2822, Vol. 8, nr 5, artikkel-id ENEURO.0141-21.2021Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Opsin 3 (Opn3) is highly expressed in the adult brain, however, information for spatial and temporal expression patterns during embryogenesis is significantly lacking. Here, an Opn3-eGFP reporter mouse line was used to monitor cell body expression and axonal projections during embryonic and early postnatal to adult stages. By applying 2D and 3D fluorescence imaging techniques, we have identified the onset of Opn3 expression, which predominantly occurred during embryonic stages, in various structures during brain/head development. In ad-dition, this study defines over twenty Opn3-eGFP-positive neural structures never reported before. Opn3-eGFP was first observed at E9.5 in neural regions, including the ganglia that will ultimately form the trigeminal, facial and vestibulocochlear cranial nerves (CNs). As development proceeds, expanded Opn3-eGFP expression coincided with the formation and maturation of critical components of the central and peripheral nervous systems (CNS, PNS), including various motor-sensory tracts, such as the dorsal column-medial lemniscus (DCML) sensory tract, and olfactory, acoustic, and optic tracts. The widespread, yet distinct, detection of Opn3-eGFP already at early embryonic stages suggests that Opn3 might play important functional roles in the developing brain and spinal cord to regulate multiple motor and sensory circuitry systems, including proprio-ception, nociception, ocular movement, and olfaction, as well as memory, mood, and emotion. This study presents a crucial blueprint from which to investigate autonomic and cognitive opsin-dependent neural development and resultant behaviors under physiological and pathophysiological conditions.

sted, utgiver, år, opplag, sider
Society for Neuroscience, 2021
Emneord
Brain, Development, Encephalopsin, Nervous system, Opn3, OPT
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-187852 (URN)10.1523/ENEURO.0141-21.2021 (DOI)000704430100013 ()34417283 (PubMedID)2-s2.0-85114912713 (Scopus ID)
Forskningsfinansiär
Swedish Research Council, 2017-01430The Kempe Foundations, SMK-1763Swedish Research Council, 2017-01307
Tilgjengelig fra: 2021-09-23 Laget: 2021-09-23 Sist oppdatert: 2023-09-05bibliografisk kontrollert
Serra-Navarro, B., Fernandez-Ruiz, R., García-Alamán, A., Pradas-Juni, M., Fernandez-Rebollo, E., Esteban, Y., . . . Gasa, R. (2021). Gsα-dependent signaling is required for postnatal establishment of a functional β-cell mass. Molecular Metabolism, 53, Article ID 101264.
Åpne denne publikasjonen i ny fane eller vindu >>Gsα-dependent signaling is required for postnatal establishment of a functional β-cell mass
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2021 (engelsk)Inngår i: Molecular Metabolism, ISSN 2212-8778, Vol. 53, artikkel-id 101264Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Objective: Early postnatal life is a critical period for the establishment of the functional β-cell mass that will sustain whole-body glucose homeostasis during the lifetime. β cells are formed from progenitors during embryonic development but undergo significant expansion in quantity and attain functional maturity after birth. The signals and pathways involved in these processes are not fully elucidated. Cyclic adenosine monophosphate (cAMP) is an intracellular signaling molecule that is known to regulate insulin secretion, gene expression, proliferation, and survival of adult β cells. The heterotrimeric G protein Gs stimulates the cAMP-dependent pathway by activating adenylyl cyclase. In this study, we sought to explore the role of Gs-dependent signaling in postnatal β-cell development.

Methods: To study Gs-dependent signaling, we generated conditional knockout mice in which the α subunit of the Gs protein (Gsα) was ablated from β-cells using the Cre deleter line Ins1Cre. Mice were characterized in terms of glucose homeostasis, including in vivo glucose tolerance, glucose-induced insulin secretion, and insulin sensitivity. β-cell mass was studied using histomorphometric analysis and optical projection tomography. β-cell proliferation was studied by ki67 and phospho-histone H3 immunostatining, and apoptosis was assessed by TUNEL assay. Gene expression was determined in isolated islets and sorted β cells by qPCR. Intracellular cAMP was studied in isolated islets using HTRF-based technology. The activation status of the cAMP and insulin-signaling pathways was determined by immunoblot analysis of the relevant components of these pathways in isolated islets. In vitro proliferation of dissociated islet cells was assessed by BrdU incorporation.

Results: Elimination of Gsα in β cells led to reduced β-cell mass, deficient insulin secretion, and severe glucose intolerance. These defects were evident by weaning and were associated with decreased proliferation and inadequate expression of key β-cell identity and maturation genes in postnatal β-cells. Additionally, loss of Gsα caused a broad multilevel disruption of the insulin transduction pathway that resulted in the specific abrogation of the islet proliferative response to insulin.

Conclusion: We conclude that Gsα is required for β-cell growth and maturation in the early postnatal stage and propose that this is partly mediated via its crosstalk with insulin signaling. Our findings disclose a tight connection between these two pathways in postnatal β cells, which may have implications for using cAMP-raising agents to promote β-cell regeneration and maturation in diabetes.

sted, utgiver, år, opplag, sider
Elsevier, 2021
Emneord
cAMP, Cell maturation, Gs, Insulin signaling, Postnatal development, Replication, β-Cell mass
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-191152 (URN)10.1016/j.molmet.2021.101264 (DOI)000704022000004 ()34091063 (PubMedID)2-s2.0-85108283081 (Scopus ID)
Tilgjengelig fra: 2022-01-10 Laget: 2022-01-10 Sist oppdatert: 2022-01-10bibliografisk kontrollert
Quilichini, E., Fabre, M., Nord, C., Dirami, T., Le Marec, A., Cereghini, S., . . . Haumaitre, C. (2021). Insights into the etiology and physiopathology of MODY5/HNF1B pancreatic phenotype with a mouse model of the human disease. Journal of Pathology, 254(1), 31-45
Åpne denne publikasjonen i ny fane eller vindu >>Insights into the etiology and physiopathology of MODY5/HNF1B pancreatic phenotype with a mouse model of the human disease
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2021 (engelsk)Inngår i: Journal of Pathology, ISSN 0022-3417, E-ISSN 1096-9896, Vol. 254, nr 1, s. 31-45Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Maturity‐onset diabetes of the young type 5 (MODY5) is due to heterozygous mutations or deletion of HNF1B. No mouse models are currently available to recapitulate the human MODY5 disease. Here, we investigate the pancreatic phenotype of a unique MODY5 mouse model generated by heterozygous insertion of a human HNF1B splicing mutation at the intron‐2 splice donor site in the mouse genome. This Hnf1bsp2/+ model generated with targeted mutation of Hnf1b mimicking the c.544+1G>T (<IVS2nt+1G>T) mutation identified in humans, results in alternative transcripts and a 38% decrease of native Hnf1b transcript levels. As a clinical feature of MODY5 patients, the hypomorphic mouse model Hnf1bsp2/+ displays glucose intolerance. Whereas Hnf1bsp2/+ isolated islets showed no altered insulin secretion, we found a 65% decrease in pancreatic insulin content associated with a 30% decrease in total large islet volume and a 20% decrease in total β‐cell volume. These defects were associated with a 30% decrease in expression of the pro‐endocrine gene Neurog3 that we previously identified as a direct target of Hnf1b, showing a developmental etiology. As another clinical feature of MODY5 patients, the Hnf1bsp2/+ pancreases display exocrine dysfunction with hypoplasia. We observed chronic pancreatitis with loss of acinar cells, acinar‐to‐ductal metaplasia, and lipomatosis, with upregulation of signaling pathways and impaired acinar cell regeneration. This was associated with ductal cell deficiency characterized by shortened primary cilia. Importantly, the Hnf1bsp2/+ mouse model reproduces the pancreatic features of the human MODY5/HNF1B disease, providing a unique in vivo tool for molecular studies of the endocrine and exocrine defects and to advance basic and translational research.

sted, utgiver, år, opplag, sider
John Wiley & Sons, 2021
Emneord
exocrine dysfunction, glucose intolerance, haploinsufficiency, HNF1B, maturity-onset diabetes of the young (MODY), optical projection tomography (OPT), pancreatic hypoplasia, pancreatitis, primary cilia, β-cells
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-181833 (URN)10.1002/path.5629 (DOI)000630230000001 ()33527355 (PubMedID)2-s2.0-85102621816 (Scopus ID)
Tilgjengelig fra: 2021-04-06 Laget: 2021-04-06 Sist oppdatert: 2022-04-19bibliografisk kontrollert
Eriksson, M., Litwak, S. A., Yun, Y., Stanley, W. J., Thorn, P., Ahlgren, U. & Gurzov, E. N. (2021). Insulin-Binding Peptide Probes Provide a Novel Strategy for Pancreatic β-Cell Imaging. Molecular Pharmaceutics, 18(12), 4428-4436
Åpne denne publikasjonen i ny fane eller vindu >>Insulin-Binding Peptide Probes Provide a Novel Strategy for Pancreatic β-Cell Imaging
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2021 (engelsk)Inngår i: Molecular Pharmaceutics, ISSN 1543-8384, E-ISSN 1543-8392, Vol. 18, nr 12, s. 4428-4436Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

Type 1 diabetes develops in childhood and adolescence, with peak incidence in the early teenage years. There is an urgent need for an accurate method to detect insulin-producing β-cells in patients that is not affected by alterations in β-cell function. As part of our research program to design specific probes to measure β-cell mass, we recently developed a novel insulin-binding peptide probe (IBPP) for the detection of β-cells in vivo. Here, we applied our innovative method to show specific labeling of this IBPP to human and mouse fixed β-cells in pancreatic islets. Importantly, we showed staining of human and mouse islets in culture without any negative functional or cell viability impact. Moreover, the IBPP-stained mouse islets after tail vein injection in vivo, albeit with batch differences in staining efficiency. In conclusion, we provide evidence showing that the IBPP can be used for future accurate detection of β-cell mass in a variety of preclinical models of diabetes.

sted, utgiver, år, opplag, sider
American Chemical Society (ACS), 2021
Emneord
glucose-stimulated insulin secretion, insulin-binding peptide, pancreatic islets, type 1 diabetes, β-cell imaging
HSV kategori
Identifikatorer
urn:nbn:se:umu:diva-189219 (URN)10.1021/acs.molpharmaceut.1c00616 (DOI)000755047200018 ()2-s2.0-85118183928 (Scopus ID)
Forskningsfinansiär
EU, FP7, Seventh Framework Programme, 289932Swedish Research CouncilNovo Nordisk
Tilgjengelig fra: 2021-11-10 Laget: 2021-11-10 Sist oppdatert: 2023-09-05bibliografisk kontrollert
Organisasjoner
Identifikatorer
ORCID-id: ORCID iD iconorcid.org/0000-0001-5923-8572