A novel nanoluciferase transgenic reporter to measure proteinuria in zebrafishCitation formats

  • External authors:
  • Emmanuel Lemarie
  • Anthony Jackson-Crawford
  • J Bernard Davenport

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A novel nanoluciferase transgenic reporter to measure proteinuria in zebrafish. / Naylor, Richard; Lemarie, Emmanuel; Jackson-Crawford, Anthony ; Davenport, J Bernard; Mironov, Aleksandr; Lowe, Martin; Lennon, Rachel.

In: Kidney International, 09.05.2022.

Research output: Contribution to journalArticlepeer-review

Harvard

Naylor, R, Lemarie, E, Jackson-Crawford, A, Davenport, JB, Mironov, A, Lowe, M & Lennon, R 2022, 'A novel nanoluciferase transgenic reporter to measure proteinuria in zebrafish', Kidney International.

APA

Naylor, R., Lemarie, E., Jackson-Crawford, A., Davenport, J. B., Mironov, A., Lowe, M., & Lennon, R. (Accepted/In press). A novel nanoluciferase transgenic reporter to measure proteinuria in zebrafish. Kidney International.

Vancouver

Naylor R, Lemarie E, Jackson-Crawford A, Davenport JB, Mironov A, Lowe M et al. A novel nanoluciferase transgenic reporter to measure proteinuria in zebrafish. Kidney International. 2022 May 9.

Author

Naylor, Richard ; Lemarie, Emmanuel ; Jackson-Crawford, Anthony ; Davenport, J Bernard ; Mironov, Aleksandr ; Lowe, Martin ; Lennon, Rachel. / A novel nanoluciferase transgenic reporter to measure proteinuria in zebrafish. In: Kidney International. 2022.

Bibtex

@article{c22b18a61486497db1431838aee7af54,
title = "A novel nanoluciferase transgenic reporter to measure proteinuria in zebrafish",
abstract = "The zebrafish is an important animal system for modelling human diseases. This includes kidney dysfunction as the embryonic kidney (pronephros) shares considerable molecular and morphological homology with the human nephron. A key clinical indicator of kidney disease is proteinuria, but a high-throughput readout of proteinuria in the zebrafish is lacking. We used the Tol2 transposon system to generate a transgenic zebrafish line that uses the fabp10a liver-specific promoter to over-express a nanoluciferase molecule fused with the D3 domain of Receptor-Associated-Protein (which we term NL-D3). Using a luminometer, we quantified proteinuria in NL-D3 zebrafish larvae by measuring the intensity of luminescence in the embryo medium. In the healthy state, NL-D3 is not excreted, but when embryos were treated with chemicals that affected either proximal tubular reabsorption (cisplatin, gentamicin) or glomerular filtration (angiotensin II, Hanks Balanced Salt Solution, Bovine Serum Albumin), NL-D3 is detected in fish medium. Similarly, depletion of several gene products associated with kidney disease (nphs1, nphs2, lrp2a, ocrl, col4a3, and col4a4) also induced NL-D3 proteinuria. Treating col4a4 depleted zebrafish larvae (a model of Alport syndrome) with captopril reduced proteinuria in this system. Our findings confirm the use of the NL-D3 transgenic zebrafish as a robust and quantifiable proteinuria reporter. Given the feasibility of high-throughput assays in zebrafish, this novel reporter will permit screening for drugs that ameliorate proteinuria, thereby prioritising candidates for further translational studies.",
author = "Richard Naylor and Emmanuel Lemarie and Anthony Jackson-Crawford and Davenport, {J Bernard} and Aleksandr Mironov and Martin Lowe and Rachel Lennon",
year = "2022",
month = may,
day = "9",
language = "English",
journal = "Kidney International",
issn = "0085-2538",
publisher = "Springer Nature",

}

RIS

TY - JOUR

T1 - A novel nanoluciferase transgenic reporter to measure proteinuria in zebrafish

AU - Naylor, Richard

AU - Lemarie, Emmanuel

AU - Jackson-Crawford, Anthony

AU - Davenport, J Bernard

AU - Mironov, Aleksandr

AU - Lowe, Martin

AU - Lennon, Rachel

PY - 2022/5/9

Y1 - 2022/5/9

N2 - The zebrafish is an important animal system for modelling human diseases. This includes kidney dysfunction as the embryonic kidney (pronephros) shares considerable molecular and morphological homology with the human nephron. A key clinical indicator of kidney disease is proteinuria, but a high-throughput readout of proteinuria in the zebrafish is lacking. We used the Tol2 transposon system to generate a transgenic zebrafish line that uses the fabp10a liver-specific promoter to over-express a nanoluciferase molecule fused with the D3 domain of Receptor-Associated-Protein (which we term NL-D3). Using a luminometer, we quantified proteinuria in NL-D3 zebrafish larvae by measuring the intensity of luminescence in the embryo medium. In the healthy state, NL-D3 is not excreted, but when embryos were treated with chemicals that affected either proximal tubular reabsorption (cisplatin, gentamicin) or glomerular filtration (angiotensin II, Hanks Balanced Salt Solution, Bovine Serum Albumin), NL-D3 is detected in fish medium. Similarly, depletion of several gene products associated with kidney disease (nphs1, nphs2, lrp2a, ocrl, col4a3, and col4a4) also induced NL-D3 proteinuria. Treating col4a4 depleted zebrafish larvae (a model of Alport syndrome) with captopril reduced proteinuria in this system. Our findings confirm the use of the NL-D3 transgenic zebrafish as a robust and quantifiable proteinuria reporter. Given the feasibility of high-throughput assays in zebrafish, this novel reporter will permit screening for drugs that ameliorate proteinuria, thereby prioritising candidates for further translational studies.

AB - The zebrafish is an important animal system for modelling human diseases. This includes kidney dysfunction as the embryonic kidney (pronephros) shares considerable molecular and morphological homology with the human nephron. A key clinical indicator of kidney disease is proteinuria, but a high-throughput readout of proteinuria in the zebrafish is lacking. We used the Tol2 transposon system to generate a transgenic zebrafish line that uses the fabp10a liver-specific promoter to over-express a nanoluciferase molecule fused with the D3 domain of Receptor-Associated-Protein (which we term NL-D3). Using a luminometer, we quantified proteinuria in NL-D3 zebrafish larvae by measuring the intensity of luminescence in the embryo medium. In the healthy state, NL-D3 is not excreted, but when embryos were treated with chemicals that affected either proximal tubular reabsorption (cisplatin, gentamicin) or glomerular filtration (angiotensin II, Hanks Balanced Salt Solution, Bovine Serum Albumin), NL-D3 is detected in fish medium. Similarly, depletion of several gene products associated with kidney disease (nphs1, nphs2, lrp2a, ocrl, col4a3, and col4a4) also induced NL-D3 proteinuria. Treating col4a4 depleted zebrafish larvae (a model of Alport syndrome) with captopril reduced proteinuria in this system. Our findings confirm the use of the NL-D3 transgenic zebrafish as a robust and quantifiable proteinuria reporter. Given the feasibility of high-throughput assays in zebrafish, this novel reporter will permit screening for drugs that ameliorate proteinuria, thereby prioritising candidates for further translational studies.

M3 - Article

JO - Kidney International

JF - Kidney International

SN - 0085-2538

ER -