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Laura Bianchi

General Information

Laura  Bianchi


  • Office: 305-243-1886
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  • English
  • Italian, English


  • Associate Professor

Research Interests

Ion channels and transporters in glia-neurons functional interaction.

Glia are the most abundant cell type in the nervous system. Until recently, glia were thought to be mere support cells for neurons with no active role in processing and propagating synaptic information.  Now, it is widely acknowledged that glia actively respond to and modulate synaptic signals.  Essential to this process are ions and other signaling molecules that are released from glia, or conversely transported into glia.  Plasma membrane channels and transporters mediate the movement of these molecules into or out of glia. We still have incomplete understanding of the influence of these membrane proteins on glial function and ultimately synapse function and animal behavior. Moreover, the molecular identities of most of these membrane proteins are still unknown. Our RNA sequencing data have identified over 30 glia-enriched membrane channels and transporters with potential roles in these processes. Using a combination of molecular, genetic, imaging and electrophysiological approaches we are testing the contribution of these channels and transporters to glial and neuronal function, and behavior.

DEG/ENaC channels in sensory perception.

DEG/ENaC ion channels (named after the C. elegansdegenerins‹the first member cloned causes degeneration-- and the mammalian epithelial Na+ channels) are two-transmembrane domain subunits of voltage-independent Na+/Ca2+ channels that come together in trimers to contribute to a wide variety of biological functions across phyla including touch sensation, pain sensation, thermo-sensation, pheromone perception, proprioception, vascular and visceral mechanotransduction, taste and transepithelial Na+ transport.

DEG/ENaC dysfunction has been linked to human diseases. For example, mutant epithelially-expressed DEG/ENaC channels cause a form of salt-sensitive hypertension called Liddle syndrome and neuronally-expressed DEG/ENaCs induce neurodegeneration in conditions in which they become hyperactivated. Based on amino acid sequence, mammalian and C. elegansDEG/ENaC channel subunits can be grouped into two subfamilies, the ASIC (Acid Sensitive Ion Channels) and the ENaC (Epithelial Na+ Channels) subfamilies. Functional differences between members of the two subfamilies include constitutive activity for ENaCs and Ca2+ permeability for ASICs. While ENaC channels function in transepithelial Na+ transport, ASICs are primarily neuronally-expressed, are opened by extracellular protons and contribute to sensory perception, and learning and memory. We have recently discovered that ENaC-like channels are expressed in C. elegans glia associated with sensory neurons and that they contribute to sensory perception.

DEG/ENaC channels functional properties and neurotoxicity.

Hyperactivated neuronal DEG/ENaC channels were shown to cause neuronal swelling and death mediated by intracellular Ca2+ overload. Interestingly, mammalian neurotoxic DEG/ENaC ASIC1a and C. elegans homolog MEC-4(d) are both Ca2+ permeable, suggesting that their calcium permeability contributes directly to elevation of intracellular calcium and is a necessary feature for their toxicity. However, of the six ASIC subunits cloned so far ASIC1a, ASIC2a and ASIC2b expressed in the brain, only homomeric ASIC1a and heteromeric ASIC1a/2b show calcium permeability. Moreover, we showed that homologous C. elegans DEG/ENaC channel UNC-8(d) is not Ca2+ permeable yet it is toxic both in vivo and in Xenopus oocytes, suggesting that Na+ influx is sufficient to induce toxicity. We are currently investigating the permeability properties that render DEG/ENaC channels toxic by expressing mutants and chimeras in Xenopus oocytes.

For more details check out our website: http://www.laura-bianchi.com


1997 PhD
University Of Florence
1992 BS/MS
University of Milan


  • Matthewman C., Miller-Fleming T. W., Miller, D. M. III. and Bianchi L. Ca2+ permeability and Na+ conductance in cellular toxicity caused by hyperactive DEG/ENaC channels. American Journal of Cell Physiology, 311(6):C920-930, 2016, PMID: 27760755.
  • Miller-Fleming T. W., Sarah C. Petersen S. C., Manning L., Matthewman C., Gornet M., Beers A., Hori S., Mitani S., Bianchi L., Richmond J., David M. Miller, D. M. III. The DEG/ENaC Cation Channel Protein UNC-8 Drives Activity-Dependent Synapse Removal in Remodeling GABAergic Neurons. eLife, Jul. 12; 5 pii: e14599, 2016. PMID: 27403890, PMCID: PMC4980115.
  • Grant J., Matthewman C., and Bianchi L. A novel mechanism of pH buffering in C. elegans glia: bicarbonate transport via the voltage-gated ClC Cl- channel CLH-1. Journal of Neuroscience 35(50): 16377-97, 2015. PMID: 26674864, PMCID: PMC4679820.
  • Zhuang G. Z., Keeler B., Grant J., Bianchi L., Fu E. S., Zhang Y. P., Erasso D. M., Cui J. G., Wiltshire T., Li Q., Hao S., Sarantopoulos K. D., Candiotti K., Wishnek S. M., Smith S. B., Maixner W., Diatchenko L., Martin E. R., Levitt R. C.?Carbonic anhydrase-8 regulates inflammatory pain by inhibiting the ITR1-cytosolic free calcium pathway. PLoS One, 10(3): e0118273,?2015. PMID: 25734498
  • Sangaletti R., Dahl G., and Bianchi L. Mechanosensitive unpaired innexin channels in C. elegans touch neurons. American Journal of Cell Physiology, 307(10): C966-77, 2014. PMID: 25252948, PMCID: PMC4233263.
  • Kamat S., Yeola S., Zhang W., Bianchi L.*, and Driscoll M*. NRA-2, a nicalin homolog, regulates neuronal death by controlling surface localization of toxic C. elegans DEG/ENaCs. Journal of Biological Chemistry, 2014, Apr 25;289(17):11916-26, PMID: 24567339, *co-corresponding authors
  • Safratowich B., Hossain M., Bianchi L., and Carvelli L. Amphetamine potentiates the effects of ß-Phenylethylamine through activation of an amine-gated chloride channel. Journal of Neuroscience, 34(13): 4686-91, 2014, PMID: 24672014, PMCID: PMC3965791.
  • Wang Y., Matthewman C., Han L., Miller T., Miller D. M. III and Bianchi L. Neurotoxic unc-8 mutants encode constitutively active DEG/ENaC channels that are blocked by divalent cations. Journal of General Physiology, 142(2): 157-69, 2013, PMID: 23898007, PMCID:PMC3727304.
  • Safratowich D. D, Lor C., Bianchi L., and Carvelli L. Amphetamine activates an amine-gated chloride channel to generate behavioral effects in Caenorhabditis elegans. Journal of Biological Chemistry, 88(30): 21630-7, 2013, PMID: 23775081, PMCID:PMC3724622.
  • Sangaletti R. and Bianchi L. A method for culturing embryonic C. elegans cells”. Jove, (79): e50649, 2013, PMID: 24084243.
  • Han L., Wang Y., Sangaletti R., D’Urso G., Lu Y., Shaham S., and Bianchi L. Two novel DEG/ENaC channel subunits expressed in glia are needed for nose-touch sensitivity in Caenorhabditis elegans. Journal of Neuroscience, 33(3): 936-949, 2013, PMID: 23325233, PMCID:PMC3711640.
  • Grant J., Tran V., Bhattacharya S. K., and Bianchi L. Ionic currents of human trabecular meshwork cells from control and glaucoma subjects. Journal of Membrane Biology, 246(2): 167-75, 2013, PMID: 23135060, PMCID: PMC3557616.
  • Wang Y., D'Urso G., and Bianchi L. Knockout of glial channel ACD-1 exacerbates sensory deficits in a C. elegans mutant by regulating calcium levels of sensory neurons. Journal of Neurophysiology, 107(1): 148-58, 2012. PMID: 21994266, PMCID: PMC3349695.
  • Bianchi L. and Diez-Sampedro A. A single amino acid change converts the sugar sensor SGLT3 into a sugar transporter. PLoS One, 5(4): e10241, 2010. PMID: 20421923, PMCID: PMC2857651.
  • Wang Y. and Bianchi L., Insights into the molecular determinants of proton inhibition in an acid-inactivated degenerins and mammalian epithelial Na+ channel. Biochemistry, 48 (42), 10005–10013, 2009. PMID: 19769407, PMCID: PMC2764801.
  • Wang Y., Apicella A. Jr, Lee S-K, Ezcurra M., Slone R. D., Goldmit M., Schafer W. R., Shaham S., Driscoll M., and Bianchi L. A glial DEG/ENaC channel functions with neuronal channel DEG-1 to mediate specific sensory functions in C. elegans. European Molecular Biology Organization (EMBO) Journal, 27(18): 2388-2399, 2008. PMID: 18701922, PMCID: PMC2543049.
  • Zhang W.*, Bianchi L.*, Lee W.-H., Wang Y., Israel S., and Driscoll M. Intersubunit interactions between mutant DEG/ENaCs induce synthetic neurotoxicity. Cell Death and Differentiation, 15(11): 1794-1803, 2008. PMID: 18670436. * co-first author.
  • Tsechpenakis G.*, Bianchi L.*, Metaxas D., and Driscoll M. A novel computational approach for simultaneous tracking and feature extraction of C. elegans populations in fluid environments. Institute of Electrical and Electronics Engineers (IEEE) Transactions in Biomedical Engineering, 55(5): 1539-1549, 2008. PMID: 18440900 * co-first author.
  • Royal D. C.*, Bianchi L.*, Royal M. A., Lizzio M. Jr., Mukherjee G., Nunez, Y. O., and Driscoll M. Temperature-sensitive mutant of the Caenorhabditis elegans neurotoxic MEC-4(d) DEG/ENaC channel identifies a site required for trafficking or surface maintenance. The Journal of Biological Chemistry, 280(51): 41976-41986, 2005. PMID: 16239217 * co-first author.
  • Bianchi L., Gerstbrein B., Frøkjær-Jensen C., Royal D. C., Mukherjee G., Royal M. A., Xue J.,Schafer W. R., and Driscoll M. The Neurotoxic MEC-4(d) DEG/ENaC sodium channel conducts calcium: implications for necrosis initiation. Nature Neuroscience, 7 (12): 1337- 1344, 2004. PMID: 15543143.
  • Bianchi L., Gerstbrein B., Frøkjær-Jensen C., Royal D. C., Mukherjee G., Royal M. A., Xue J.,Schafer W. R., and Driscoll M. The Neurotoxic MEC-4(d) DEG/ENaC sodium channel conducts calcium: implications for necrosis initiation. Nature Neuroscience, 7 (12): 1337- 1344, 2004. PMID: 15543143.
  • Suzuki H., Kerr R., Bianchi L., Frøkjær-Jensen C., Slone D., Xue J., Gerstbrein B., Driscoll M.,and Schafer W. R. In vivo imaging of C. elegans mechanosensory neurons demonstrates a specific role for the MEC-4 channel in the process of gentle touch sensation. Neuron, 39(6):1005-1017, 2003. PMID: 12971899.
  • Bianchi L., Kwok S. K., Driscoll M., and Sesti F. A potassium channel-MiRP complex controls neurosensory function in Caenorhabditis elegans. The Journal of Biological Chemistry, 278: 12415-12424, 2003. PMID: 12533541.
  • Rutledge E., Bianchi L., Christensen M., Boehmer C., Morrison R., Broslat A., Beld A. M., George A. L. Jr., Greenstein D., and Strange K. CLH-3, a ClC-2 anion channel ortholog activated during meiotic maturation in C. elegans oocytes. Current Biology, 11 (3): 161-170, 2001. PMID: 11231150.
  • Bianchi L., Miller D. M. 3rd, and George A. L. Jr. Expression of a CIC chloride channel in Caenorhabditis elegans gamma-aminobutyric acid-ergic neurons. Neuroscience Letters, 299 (3): 177-180, 2001. PMID: 11165764.
  • Bianchi L., Priori S. G., Napolitano C., Surewicz, K. A., Dennis A. T., Memmi M., Schwartz P. J., and Brown A. M. Mechanisms of IKs suppression in LQT1 mutants. American Journal of Physiology, 279: H3003-H3011, 2000. PMID: 11087258.
  • Napolitano C., Schwartz P. J., Brown A. M., Ronchetti E., Bianchi L., Pinnavaia A., Acquaro G., and Priori S. G. Evidence for a cardiac ion channel mutation underlying drug-induced QT prolongation and life-threatening arrhythmias. Journal of Cardiovascular Electrophysiology, 11 (6): 691-696, 2000. PMID: 10868744.
  • Emmi A., Wenzel H. J., Schwartzkroin P. A., Taglialatela M., Castaldo P., Bianchi L., Nerbonne J., Robertson G. A., and Janigro D. Do glia have heart? Expression and functional role for ether-a-go-go currents in hippocampal astrocytes. Journal of Neuroscience, 20 (10): 3915-3925, 2000. PMID: 10804231.
  • Bianchi L., Priori S. G., Shen Z.-J., Dennis A. T., Napolitano C., Ronchetti E., Bryskin R., Schwartz P. J., and Brown A. M. Cellular dysfunction of LQT5-minK mutants: abnormalities of IKs, IKr and trafficking in LQT syndrome. Human Molecular Genetics, 8 (8): 1499-1507, 1999. PMID: 10400998.
  • Schwalbe R.A., Bianchi L., Accili E.A., and Brown A.M. Functional consequences of ROMK mutants linked to antenatal Bartter’s syndrome and implications for treatment. Human Molecular Genetics, 7 (6): 975-980, 1998. PMID: 9580661.
  • Priori, S. G., Schwartz, P. J., Napolitano, C., Bianchi. L., Dennis, A., De Fusco M., Brown A. M., and Casari, G. A recessive variant of the Romano-Ward syndrome? Circulation, 97(24): 2420-2425, 1998. PMID: 9641694.
  • Bianchi L., Wible B., Arcangeli A., Taglialatela M., Morra F., Castaldo P., Crociani O., Rosati B., Faravelli L., Olivotto M., and Wanke E. Herg encodes a K+ channel highly conserved in tumors of different histogenesis: a selective advantage for cancer cells? Cancer Research, 58(4): 815-822, 1998. PMID: 9485040.
  • Schwalbe R.A., Bianchi L., and Brown A.M. Mapping the kidney potassium channel ROMK1. Glycosylation of the pore signature sequence and the C-terminus. The Journal of Biological Chemistry, 272(40): 25217-25223, 1997. PMID: 9312136.
  • Guatteo E., Bianchi L., Faravelli L., Verotta L., Pellizoni F., Rogers C. B., and Wanke E. A novel K+ channel blocker isolated from “Hiccup Nut” toxin. Neuroreport, 7(15-17): 2575-2579, 1996. PMID: 8981426.
  • Schwalbe R. A., Wang Z., Bianchi L., and Brown A. M. Novel sites of N-glycosylation in ROMK1 reveal the putative pore-forming segment H5 as extracellular. The Journal of Biological Chemistry, 271: 24201-24206, 1996. PMID: 8798662
  • Arcangeli A., Faravelli L., Bianchi L., Rosati B., Gritti A., Vescovi A., Wanke E., and Olivotto M. Soluble or bound laminin elicits in human neuroblastoma cells short-or long-term potentiation of a K+ inwardly rectifying current: relevance to neuritogenesis. Cell Adhesion and Communication, 4(4-5): 369-385, 1996. PMID: 9117354
  • Bianchi L.*, Roy M. L.*, Taglialatela M., Lundgren D.W., Brown A.M., and Ficker E. Regulation by spermine of native inward rectifier K+ channels in RBL-1 cells. The Journal of Biological Chemistry, 271: 6114-6121, 1996. PMID: 8626398 * co-first author.
  • Arcangeli A., Bianchi L., Becchetti A., Faravelli L., Coronello M., Mini E., Olivotto M., and Wanke E. A novel inward-rectifying K+ current with a cell-cycle dependence governs the resting potential of mammalian neuroblastoma cells. The Journal of Physiology, 489: 455- 471, 1996. PMID: 8847640.
  • Bianchi L., Arcangeli A., Bartolini P., Mugnai G., Wanke E., and Olivotto M. An inward rectifier K+ current modulates in neuroblastoma cells the tyrosine phosphorylation of the pp125FAK and associates proteins: role in neuritogenesis. Biochemical and Biophysical Research Communications, 210(3): 823-829, 1995. PMID: 7539261.
  • Wanke E., Bianchi L., Mantegazza M., Guatteo E., Mancinelli E., and Ferroni A. Muscarinic regulation of Ca2+ currents in rat sensory neurons: channel and receptor types, doseresponse relationships and cross-talk pathways. European Journal of Neuroscience, 6(3): 381-391, 1994. PMID: 8019675.


 Laura Bianchi

University of Florence, Italy; PhD in Physiology; May 1997

University of Milan, Italy, BS/MS in Biochemistry, 1990-1992



Department of Physiology and Biophysics, University of Miami, Miami, FL, Associate Professor, 2013-present. Tenured, June 2015-present.              


Department of Physiology and Biophysics, University of Miami, Miami, FL, Assistant Professor (tenure-earning track), 2006-2013.                 


Department of Molecular Biology and Biochemistry, Rutgers University, Piscataway, NJ, Assistant Professor (research track), 2001-2006.                 


Department of Medicine, Vanderbilt University, Nashville, TN, Postdoctoral Research Fellow, (Supervisor: Alfred L. George Jr.), 1998-2001.